Escape of deer shows Wisconsin is failing to protect wild herd
By Paul A. Smith of the Journal Sentinel
Sept. 16, 2015 9:08 p.m. An Eau Claire County deer farm is back in the
spotlight for the wrong reason.
And with the scrutiny comes a growing realization: Wisconsin agencies are
bungling their responsibilities to protect the state's multibillion-dollar wild
deer herd.
The Eau Claire County deer farm made news in June when a 7-year-old doe at
the facility tested positive for chronic wasting disease. The Department of
Agriculture, Trade and Consumer Protection — which has responsibility over deer
farms in Wisconsin — initiated a plan to kill the 167 deer remaining at the
facility.
But the depopulation did not happen. In fact, the captive herd increased by
nearly 50% with the birth of fawns.
The story faded to the background until earlier this week when sources
notified the Milwaukee Journal Sentinel that 12 deer escaped the facility on
Sept. 9.
The deer, all 2-year-old bucks, may have gotten out through an open gate,
Department of Natural Resources officials said Wednesday.
Just nine of the deer were captured, according to DATCP.
Neither DATCP nor the DNR announced the deer escape to the public.
"It's outrageous," said Mark Noll of Alma, a hunter, farmer and longtime
member of the Wisconsin Conservation Congress. "It's like someone decided
they've thrown in the towel on chronic wasting disease and they're too
embarrassed to talk about what's happening."
The farm was not depopulated because "federal indemnity funds were not
available in this fiscal year," said Paul McGraw, state veterinarian for
DATCP.
While state officials waited for federal help over the last several months,
no special fencing or other additional structures were put in place to prevent
escapes and reduce the risk of disease spread to wild deer in the area.
"Biosecurity on cervid farms is a joke," said Dave Clausen of Amery, a
retired veterinarian and former chairman of the Wisconsin Natural Resources
Board.
Infectious abnormal proteins can come in and out of deer farms when animals
escape, when animals are transported between facilities and when mud, dust or
other material is carried on vehicle tires or even the soles of shoes, Clausen
said.
State officials said Wednesday it wasn't clear if the farm owner, Rick
Vojtik of Fairchild, will face a penalty for the escaped deer.
Noll said state officials should have at least alerted the public to the
escape and asked for assistance in locating and possibly killing the deer. The
bucks are wearing ear tags, according to DATCP. The Wisconsin archery and
crossbow seasons opened Saturday for deer. Hunters in the area would likely have
been happy to help in the effort.
Chronic wasting disease was first detected in southern Wisconsin in 2002.
It is now found in more than 40% of adult bucks in parts of Iowa County.
But more than half the counties in the state have never had a CWD-positive
deer. The diseased doe found in June was the first in Eau Claire County.
For the benefit of deer hunting and the wild deer herd, it's critical to
prevent new hot spots of the disease.
The wild deer resource in Wisconsin is responsible for between $1 billion
and $4 billion in annual economic activity in Wisconsin, based on various
estimates.
Under Wisconsin law, DATCP has responsibility for captive cervid farms
"inside the fence" while DNR has responsibility for the fence and deer outside
of it.
DNR officials said Wednesday the facility's fence was checked in May and
found to be in "good working condition."
The escape of deer from a CWD-positive facility in Eau Claire County was
depressing news to Noll, who lives in nearby Buffalo County, an internationally
renowned deer hunting destination.
"The system is not working," Noll said. "If this is how we're going to run
deer farms and game farms, it's a failure and people need to wake up."
Also of significance: The Eau Claire County deer farm is about 25 miles
from the recently-released elk herd in Jackson County's Black River State
Forest. The elk were allowed to be imported from Kentucky in large part because
that state's herd has never had a CWD-positive animal.
It's not known how many other deer at the Eau Claire County facility — if
any — have CWD. But it is well documented that transmissible diseases are passed
more readily when animals are in close quarters or direct contact.
With the addition of this year's fawn crop, the Eau Claire County farm has
about 245 deer on 10 acres, DATCP officials said on Wednesday.
Last October, 284 of 356 (80%) of deer on an Iowa deer farm were found to
be CWD-positive.
The disease percolated at the facility for at least two years as litigation
delayed depopulation. In the end, the Iowa deer farm owners received $917,100 in
federal indemnity funding from the U.S. Department of Agriculture.
Neither DATCP nor DNR officials advanced any new plan for dealing with the
Eau Claire County deer farm. The two state agencies said Wednesday they "are
reviewing the situation to determine the appropriate course of action."
This month's incident is not the first escape of deer from the farm this
year. Two deer remain on the loose since May when a tree fell on a fence at the
facility.
"The agencies have responsibilities to the public and to the resource,"
Clausen said. "They are not living up to their end of the bargain, not by a long
shot."
Send email to psmith@journalsentinel.com
© 2015, Journal Sentinel Inc. All rights reserved.
News Releases Return...
Walworth County deer farmer penalized for violating quarantines
August 20, 2015
Walworth County deer farmer penalized for violating quarantines (PDF)
Contact: Raechelle Belli, 608-224-5005 or Bill Cosh, Communications
Director, 608-224-5020
MADISON -- A Walworth County farm-raised deer keeper agreed to a civil
forfeiture for violating quarantines imposed to manage the spread of chronic
wasting disease (CWD). The quarantines were issued in February 2007 and
September 2008, the State Veterinarian’s office said today.
In a plea agreement, Dana Montana, owner of Lake Geneva Animal Gardens,
agreed to a settlement without further litigation. Montana has agreed to pay a
total of $8,000 to Walworth County Circuit Court including court costs and fees
by December 31, 2015.
“Animal disease control is a priority for this department so the rules
exist for a good reason,” said State Veterinarian Dr. Paul McGraw. “We impose
quarantines to ensure that diseases like CWD do not spread.”
Quarantine of animals and animal products is one of the most important
Department orders to protect animal and public health. Similar quarantines were
imposed during the recent avian influenza outbreak that led to the destruction
of nearly two million chickens and turkeys in Wisconsin. Without the
quarantines, many more birds may have had to be destroyed due to infection.
The quarantines explicitly forbid the owner from moving deer from her
property without prior written permission from the Wisconsin Department of
Agriculture, Trade and Consumer Protection. An inspection of records and further
investigation identified the violation that led to the charges.
“Our animal health laws are in place to protect animal health and the
industry,” McGraw said. “In general, the farm-raised deer industry has been
compliant with quarantines, which helps to protect other farms and wild deer
from the spread of CWD. When a farm fails to follow the law, we take it
seriously.”
Connect with us on Twitter at twitter.com/widatcp or Facebook at
facebook.com/widatcp.
# # #
Wednesday, March 04, 2015
*** Disease sampling results provide current snapshot of CWD in Wisconsin
finding 324 positive detections statewide in 2014
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
http://chronic-wasting-disease.blogspot.com/2015/07/two-escaped-captive-deer-on-loose-in.html
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
Friday, February 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary
et al
Monday, January 16, 2012
9 GAME FARMS IN WISCONSIN TEST POSITIVE FOR CWD
Saturday, February 04, 2012
Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol
Needs To Be Revised
Wisconsin : 436 Deer Have Escaped From Farms to Wild
Date: March 18, 2003 Source: Milwaukee Journal Sentinel
Contacts: LEE BERGQUIST lbergquist@journalsentinel.com
State finds violations, lax record keeping at many sites, report says A
state inspection of private deer farms, prompted by the discovery of chronic
wasting disease, found that 436 white-tailed deer escaped into the wild,
officials said Tuesday
The Department of Natural Resources found that captive deer have escaped
from one-third of the state's 550 deer farms over the lifetime of the
operations. The agency also uncovered hundreds of violations and has sought a
total of 60 citations or charges against deer farm operators.
Hundreds of deer escape
The DNR found a total of 671 deer that escaped farms - 436 of which were
never found - because of storm-damaged fences, gates being left open or the
animals jumping over or through fences.
In one example in Kewaunee County, a deer farmer's fence was knocked down
in a summer storm. Ten deer escaped, and the farmer told the DNR he had no
intention of trying to reclaim them. The DNR found five of the deer, killed them
and cited the farmer for violation of a regulation related to fencing.
Another deer farmer near Mishicot, in Manitowoc County, released all nine
of his whitetails last summer after he believed the discovery of chronic wasting
disease was going to drive down the market for captive deer.
The DNR found 24 instances of unlicensed deer farms and issued 19
citations.
Game Farms Inspected
A summary of the findings of the Department of Natural Resources'
inspection of 550 private white-tailed deer farms in the state: The deer farms
contained at least 16,070 deer, but the DNR believes there are more deer in
captivity than that because large deer farms are unable to accurately count
their deer. 671 deer had escaped from game farms, including 436 that were never
found.
24 farmers were unlicensed. One had been operating illegally since 1999
after he was denied a license because his deer fence did not meet minimum
specifications
Records maintained by operators ranged from "meticulous documentation to
relying on memory." At least 227 farms conducted various portions of their deer
farm business with cash. Over the last three years, 1,222 deer died on farms for
various reasons. Disease testing was not performed nor required on the majority
of deer. Farmers reported doing business with people in 22 other states and one
Canadian province. ..
using a cwd tse prion test that is not 100% validated at all times, of all
age groups, is just asking for trouble. either false positives or false
negatives. I am for a cwd tse prion test as much as the next person, but if not
validated properly, you will have bigger problems. until that, in my opinion,
scorched earth policy is the only way to be sure. ...
Saturday, September 12, 2015
*** In utero transmission and tissue distribution of chronic wasting
disease-associated prions in free-ranging Rocky Mountain elk ***
>>>Interestingly, five of fifteen sPMCA positive dams showed no
evidence of PrPCWD in either CNS or LRS, sites typically assessed in diagnosing
CWD. Analysis of fetal tissues harvested from the fifteen sPMCA positive dams
revealed PrPCWD in 80% of fetuses (12/15), regardless of gestational stage.
These findings demonstrate that PrPCWD is more abundant in peripheral tissues of
CWD exposed elk than current diagnostic methods suggest, and that transmission
of prions from mother to offspring may contribute to the efficient transmission
of the CWD in naturally exposed cervid populations.<<<
Sunday, September 13, 2015
*** urine, feces, and chronic wasting disease cwd tse prion risk factors,
loading up the environment ***
Friday, August 28, 2015
*** Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical
infection ***
Sunday, September 13, 2015
TEXAS DETECTS MORE DEER POSITIVE FOR CHRONIC WASTING DISEASE CWD tested at
a Tier 1 facility (a facility that either sold to or purchased directly from the
index facility)
Tuesday, September 15, 2015
***Texas TAHC Chronic Wasting Disease Confirmed in Lavaca County Captive
White-tailed Deer; Linked to Index Herd ***
TEXAS DEER CZAR SENT TO WISCONSIN TO SOLVE CWD CRISIS, WHILE ROME (TEXAS)
BURNS
Tuesday, August 11, 2015
Wisconsin doing what it does best, procrastinating about CWD yet again
thanks to Governor Walker
*** RAW, UNCUT, AND UNCENSORED
Sunday, August 23, 2015
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig
and take her to the dance in Texas
*** 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.
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)
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.
================================================
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
=================================================
Tuesday, June 11, 2013
CWD GONE WILD, More cervid escapees from more shooting pens on the loose in
Pennsylvania
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” page 26.
Wednesday, September 04, 2013
cwd - cervid captive livestock escapes, loose and on the run in the wild...
Tuesday, October 21, 2014
Texas Pair Convicted in Illegal Deer Breeding Operation TPWD
Thursday, August 20, 2015
TEXAS CAPTIVE Deer Industry, Pens, Breeding, Big Business, Invites Crooks
and CWD
Tuesday, September 15, 2015
Deer-trafficking scheme nets record $1.6 million fine herds not certified
to be free from chronic wasting disease, tuberculosis and brucellosis
================================================
Contamination of Plants with Prions Excreted in Urine and Feces
Under natural conditions, it is likely that the main source of prions in
the environment comes from secretory and excretory fluids, such as saliva,
urine, and feces. We and others have shown that PrPSc is released in these
fluids and excretions in various animal species (Gonzalez-Romero et al., 2008;
Haley et al., 2009, 2011; Maddison et al., 2010; Terry et al., 2011; Moda et
al., 2014). It has been estimated that the amount of infectious prions spread by
excreta during the animals’ lifespan could match or even surpass the quantity
present in the brain of a symptomatic individual (Tamgu¨ ney et al., 2009). To
study whether plant tissue can be contaminated by waste products excreted from
prion-infected hamsters and deer, leaves and roots were incubated with samples
of urine and feces and the presence of PrPSc analyzed by serial rounds of PMCA.
For these experiments, plant tissues were incubated for 1 hr with urine or feces
homogenates obtained either from 263K-infected hamsters or CWD-affected cervids.
This time was chosen because longer incubation with these biological fluids
affected the integrity of the plant tissue. After being thoroughly washed and
dried, PrPSc attached to leaves and roots was detected by PMCA. The results
clearly show that PrPSc was readily detectable after three or four rounds of
PMCA in samples of wheat grass leaves and roots exposed to both urine and feces
from 263K sick hamsters (Figure 3A) and CWD-affected cervids (Figure 3B).
Comparing these results with studies of the direct detection of PrPSc in urine
and feces (Figures 3A and 3B), it seems that the majority of PrPSc present in
these waste products was effectively attached to leaves and roots. No signal was
observed in plant tissue exposed to urine or feces coming from non-infected
hamsters.
Prions Bind to Living Plants
To investigate a more natural scenario for prion contamination of living
plants, we sprayed the leaves of wheat grass with a preparation containing 1%
263K hamster brain homogenate. Plants were let to grow for different times after
exposure, and PrPSc was detected in the leaves by PMCA in duplicates for each
time point. The results show that PrPSc was able to bind to leaves and remained
attached to the living plants for at least 49 days after exposure (Figure 4).
Considering that PrPSc signal was detectable normally in the second or third
round of PMCA without obvious trend in relation to time, we conclude that the
relative amount of PrPSc present in leaves did not appear to change
substantially over time. These data indicate that PrPSc can be retained in
living plants for at least several weeks after a simple contact with prion
contaminated materials, and PrPSc remains competent to drive prion replication.
DISCUSSION
This study shows that plants can efficiently bind prions contained in brain
extracts from diverse prion infected animals, including CWD-affected cervids.
PrPSc attached to leaves and roots from wheat grass plants remains capable of
seeding prion replication in vitro. Surprisingly, the small quantity of PrPSc
naturally excreted in urine and feces from sick hamster or cervids was enough to
efficiently contaminate plant tissue. Indeed, our results suggest that the
majority of excreted PrPSc is efficiently captured by plants’ leaves and roots.
Moreover, leaves can be contaminated by spraying them with a prion-containing
extract, and PrPSc remains detectable in living plants for as long as the study
was performed (several weeks). Remarkably, prion contaminated plants transmit
prion disease to animals upon ingestion, producing a 100% attack rate and
incubation periods not substantially longer than direct oral administration of
sick brain homogenates. Finally, an unexpected but exciting result was that
plants were able to uptake prions from contaminated soil and transport them to
aerial parts of the plant tissue. Although it may seem farfetched that plants
can uptake proteins from the soil and transport it to the parts above the
ground, there are already published reports of this phenomenon (McLaren et al.,
1960; Jensen and McLaren, 1960; Paungfoo-Lonhienne et al., 2008). The high
resistance of prions to degradation and their ability to efficiently cross
biological barriers mayplay a role in this process. The mechanism by which
plants bind, retain, uptake, and transport prions is unknown. Weare currently
studying the way in which prions interact with plants using purified,
radioactively labeled PrPSc to determine specificity of the interaction,
association constant, reversibility, saturation, movement, etc.
Epidemiological studies have shown numerous instances of scrapie or CWD
recurrence upon reintroduction of animals on pastures previously exposed to
prion-infected animals. Indeed, reappearance of scrapie has been documented
following fallow periods of up to 16 years (Georgsson et al., 2006), and
pastures were shown to retain infectious CWD prions for at least 2 years after
exposure (Miller et al., 2004). It is likely that the environmentally mediated
transmission of prion diseases depends upon the interaction of prions with
diverse elements, including soil, water, environmental surfaces, various
invertebrate animals, and plants.
However, since plants are such an important component of the environment
and also a major source of food for many animal species, including humans, our
results may have far-reaching implications for animal and human health.
Currently, the perception of the risk for animal-to-human prion transmission has
been mostly limited to consumption or exposure to contaminated meat; our results
indicate that plants might also be an important vector of transmission that
needs to be considered in risk assessment.
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
The infectious agents responsible for transmissible spongiform
encephalopathy (TSE) are notoriously resistant to most physical and chemical
methods used for inactivating pathogens, including heat. It has long been
recognized, for example, that boiling is ineffective and that higher
temperatures are most efficient when combined with steam under pressure (i.e.,
autoclaving). As a means of decontamination, dry heat is used only at the
extremely high temperatures achieved during incineration, usually in excess of
600°C. It has been assumed, without proof, that incineration totally inactivates
the agents of TSE, whether of human or animal origin.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Histochemical analysis of hamster brains inoculated with the solid residue
showed typical spongiform degeneration and vacuolation. Re-inoculation of these
brains into a new cohort of hamsters led to onset of clinical scrapie symptoms
within 75 days, suggesting that the specific infectivity of the prion protein
was not changed during the biodiesel process. The biodiesel reaction cannot be
considered a viable prion decontamination method for MBM, although we observed
increased survival time of hamsters and reduced infectivity greater than 6 log
orders in the solid MBM residue. Furthermore, results from our study compare for
the first time prion detection by Western Blot versus an infectivity bioassay
for analysis of biodiesel reaction products. We could show that biochemical
analysis alone is insufficient for detection of prion infectivity after a
biodiesel process.
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
The data presented here demonstrate that sPMCA can detect low levels of
PrPCWD in the environment, corroborate previous biological and experimental data
suggesting long term persistence of prions in the environment2,3 and imply that
PrPCWD accumulation over time may contribute to transmission of CWD in areas
where it has been endemic for decades. This work demonstrates the utility of
sPMCA to evaluate other environmental water sources for PrPCWD, including
smaller bodies of water such as vernal pools and wallows, where large numbers of
cervids congregate and into which prions from infected animals may be shed and
concentrated to infectious levels.
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
In this article the development and parameterization of a quantitative
assessment is described that estimates the amount of TSE infectivity that is
present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for
cattle and classical/atypical scrapie for sheep and lambs) and the amounts that
subsequently fall to the floor during processing at facilities that handle
specified risk material (SRM). BSE in cattle was found to contain the most oral
doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to
a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep
infected with classical and atypical scrapie, respectively. Lambs contained the
least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie
and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity
falling to the floor and entering the drains from slaughtering a whole carcass
at SRM facilities were found to be from cattle infected with BSE at rendering
and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate
plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and
collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains
are from lambs infected with classical and atypical scrapie at intermediate
plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO
ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key
inputs for the model in the companion paper published here.
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
Monday, November 3, 2014
Persistence of ovine scrapie infectivity in a farm environment following
cleaning and decontamination
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.
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
P.97: 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
Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and
Robert Kunkle1 1National Animal Disease Center; Ames, IA USA; 2Iowa State
University; Ames, IA USA
The purpose of this work was to determine susceptibility of white-tailed
deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to
that of the original inoculum and chronic wasting disease (CWD). We inoculated
WTD by a natural route of exposure (concurrent oral and intranasal (IN); n D 5)
with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc
accumulation. PrPSc was detected in lymphoid tissues at preclinical time points,
and deer necropsied after 28 months post-inoculation had clinical signs,
spongiform encephalopathy, and widespread distribution of PrPSc in neural and
lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular
profiles. WB on cerebral cortex had a profile similar to the original scrapie
inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc
with a higher profile resembling CWD. Homogenates with the 2 distinct profiles
from WTD with clinical scrapie were further passaged to mice expressing cervid
prion protein and intranasally to sheep and WTD. In cervidized mice, the 2
inocula have distinct incubation times. Sheep inoculated intranasally with WTD
derived scrapie developed disease, but only after inoculation with the inoculum
that had a scrapie-like profile. The WTD study is ongoing, but deer in both
inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary,
this work demonstrates that WTD are susceptible to the agent of scrapie, 2
distinct molecular profiles of PrPSc are present in the tissues of affected
deer, and inoculum of either profile readily passes to deer.
I strenuously once again urge the FDA and its industry constituents, to
make it MANDATORY that all ruminant feed be banned to all ruminants, and this
should include all cervids as soon as possible for the following
reasons...
======
In the USA, under the Food and Drug Administrations 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.
======
31 Jan 2015 at 20:14 GMT
*** Ruminant feed ban for cervids in the United States? ***
31 Jan 2015 at 20:14 GMT
Australia
COMMONWEALTH OF AUSTRALIA Official Committee Hansard SENATE RURAL AND
REGIONAL AFFAIRS AND TRANSPORT REFERENCES COMMITTEE Reference: Import
restrictions on beef FRIDAY, 5 FEBRUARY 2010 CANBERRA BY AUTHORITY OF THE
SENATE
RRA&T 2 Senate Friday, 5 February 2010 RURAL AND REGIONAL AFFAIRS AND
TRANSPORT
[9.03 am]
BELLINGER, Mr Brad, Chairman, Australian Beef Association
CARTER, Mr John Edward, Director, Australian Beef Association
CHAIR—Welcome. Would you like to make an opening statement?
Mr Bellinger—Thank you. The ABA stands by its submission, which we made on
14
December last year, that the decision made by the government to allow the
importation of beef from BSE affected countries is politically based, not
science based. During this hearing we will bring forward compelling new evidence
to back up this statement. When I returned to my property after the December
hearing I received a note from an American citizen. I will read a small excerpt
from the mail he sent me in order to reinforce the dangers of allowing the
importation of beef from BSE affected countries. I have done a number of press
releases on this topic, and this fellow has obviously picked my details up from
the internet. His name is Terry Singeltary and he is from Bacliff, Texas. He
states, and rightfully so:
snip...end
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics
of BSE in Canada Singeltary reply ;
Saturday, September 12, 2015
The Canadian Management of Bovine Spongiform Encephalopathy in Historical
and Scientific Perspective, 1990-2014
>>>We propose that Canadian policies largely ignored the implicit
medical nature of BSE, treating it as a purely agricultural and veterinary
issue. In this way, policies to protect Canadians were often delayed and
incomplete, in a manner disturbingly reminiscent of Britain’s failed management
of BSE. Despite assurances to the contrary, it is premature to conclude that BSE
(and with it the risk of variant Creutzfeldt-Jakob disease) is a thing of
Canada’s past: BSE remains very much an issue in Canada’s present.
<<<
Thursday, September 10, 2015
FDA TSE PRION MAD COW CIRCUS AND TRAVELING ROAD SHOW (their words, not
mine)
25th Meeting of the Transmissible Spongiform Encephalopathies Advisory
Committee Food and Drug Administration Silver Spring, Maryland June 1,
2015
Tuesday, August 4, 2015
*** FDA U.S. Measures to Protect Against BSE ***
Thursday, August 13, 2015
Iatrogenic CJD due to pituitary-derived growth hormone with genetically
determined incubation times of up to 40 years
Alzheimer's, iatrogenic, transmissible, tse, prion, what if ?
Wednesday, September 9, 2015
Evidence for human transmission of amyloid-β pathology and cerebral amyloid
angiopathy
Wednesday, September 2, 2015
Clinically Unsuspected Prion Disease Among Patients With Dementia Diagnoses
in an Alzheimer’s Disease Database
Tuesday, September 1, 2015
*** Evidence for α-synuclein prions causing multiple system atrophy in
humans with parkinsonism
*** Self-Propagative Replication of Ab Oligomers Suggests Potential
Transmissibility in Alzheimer Disease
Received July 24, 2014; Accepted September 16, 2014; Published November 3,
2014
Singeltary comment Self-Propagative Replication of Ab Oligomers Suggests
Potential Transmissibility in Alzheimer Disease ;
Monday, August 17, 2015
FDA Says Endoscope Makers Failed to Report Superbug Problems OLYMPUS
*** I told Olympus 15 years ago about these risk factors from endoscopy
equipment, disinfection, even spoke with the Doctor at Olympus, this was back in
1999. I tried to tell them that they were exposing patients to dangerous
pathogens such as the CJD TSE prion, because they could not properly clean them.
even presented my concern to a peer review journal GUT, that was going to
publish, but then it was pulled by Professor Michael Farthing et al... see
;
Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes
contaminated during neurosurgery.
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological
Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a
middle aged woman with progressive dementia were previously implicated in the
accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger
patients. The diagnoses of CJD have been confirmed for all three cases. More
than two years after their last use in humans, after three cleanings and
repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were
implanted in the cortex of a chimpanzee. Eighteen months later the animal became
ill with CJD. This finding serves to re-emphasise the potential danger posed by
reuse of instruments contaminated with the agents of spongiform
encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Singeltary et al
Posted by flounder on 03 Jul 2015 at 16:53 GMT
re-Human Prion Diseases in the United States
Posted by flounder on 01 Jan 2010 at 18:11 GMT
*** Creutzfeldt-Jakob Disease *** Public Health Crisis VIDEO
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14,
2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1
reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD)
has been stable since 1985. These estimates, however, are based only on reported
cases, and do not include misdiagnosed or preclinical cases. It seems to me that
misdiagnosis alone would drastically change these figures. An unknown number of
persons with a diagnosis of Alzheimer disease in fact may have CJD, although
only a small number of these patients receive the postmortem examination
necessary to make this diagnosis. Furthermore, only a few states have made CJD
reportable. Human and animal transmissible spongiform encephalopathies should be
reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob
disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
TSS
No comments:
Post a Comment
Note: Only a member of this blog may post a comment.