Risk behaviors in a rural community with a known point-source exposure to chronic wasting disease
Chronic Wasting Disease Human-Exposure Study
While public health agencies continue to point out that there has been no
known incident of chronic wasting disease developing in humans, a group of
people known to have been exposed to venison from a CWD-infected deer is under
study by a team of researchers from the Laboratory of Biomedical Anthropology
and Neuroscience at the State University of New York at Binghamton.
The Oneida County (New York) Chronic Wasting Disease Surveillance Project
was launched in 2005 in response to exposure to an infected deer at a March 2005
sportsmen's feast in Upstate New York. Eighty-one exposed individuals
participated in the 2005 baseline data collection, and were sent follow-up
questionnaires following each deer hunting season between 2005 and 2011.
According to researchers, over that six year period participants reported a
reduction in overall venison consumption. However, they reported no significant
changes in health conditions other than those normally associated with aging,
such as vision loss, heart disease, type 2 diabetes, weight changes,
hypertension and arthritis.
>>>over that six year period participants reported a reduction in
overall venison consumption. However, they reported no significant changes in
health conditions other than those normally associated with aging, such as
vision loss, heart disease, type 2 diabetes, weight changes, hypertension and
arthritis. <<<
PLEASE NOTE ;
At a hearing in Parliament last Wednesday, the Science and Technology
Committee was told that vCJD continued to pose a “significant” risk to UK public
health and that more than one in every 2000 people could be silent carriers of
the disease. *** vCJD can have an incubation period of over 30 years.
...tss
*** In some cases, the incubation period may be as long as 50 years
Research Open Access
Risk behaviors in a rural community with a known point-source exposure to
chronic wasting disease
Ralph M Garruto*1,2, Chris Reiber2, Marta P Alfonso2, Heidi Gastrich2,
Kelsey Needham2, Sarah Sunderman2, Sarah Walker2, Jennifer Weeks2,3, Nicholas
DeRosa4, Eric Faisst3,4, John Dunn4, Kenneth Fanelli4 and Kenneth
Shilkret4
Address: 1Laboratory of Biomedical Anthropology and Neurosciences, State
University of New York at Binghamton, PO Box 6000, Binghamton, New York,
13902-6000, USA, 2Graduate Program in Biomedical Anthropology, State University
of New York at Binghamton, PO Box 6000, Binghamton, New York, 13902-6000, USA,
3Madison County Health Department, Wampsville, New York, 13163, USA and 4Oneida
County Health Department, Utica, New York, 13501, USA
Email: Ralph M Garruto* - rgarruto@binghamton.edu; Chris Reiber -
creiber@binghamton.edu; Marta P Alfonso - madurruty@yahoo.com; Heidi Gastrich -
hj.gastrich@gmail.com; Kelsey Needham - kneedha1@binghamton.edu; Sarah Sunderman
- ssunder2@binghamton.edu; Sarah Walker - swalker4@binghamton.edu; Jennifer
Weeks - jennifer.weeks@co.madison.ny.us; Nicholas DeRosa - nderosa@ocgov.net;
Eric Faisst - eric.faisst@co.madison.ny.us; John Dunn - jdunn@ocgov.net; Kenneth
Fanelli - kfanelli@ocgov.net; Kenneth Shilkret - kshilkret@ocgov.net *
Corresponding author
Abstract
Background: The emergence and continuing spread of Chronic Wasting Disease
(CWD) in cervids has now reached 14 U.S. states, two Canadian provinces, and
South Korea, producing a potential for transmission of CWD prions to humans and
other animals globally. In 2005, CWD spread for the first time from the Midwest
to more densely populated regions of the East Coast. As a result, a large cohort
of individuals attending a wild game feast in upstate New York were exposed to a
deer that was subsequently confirmed positive for CWD.
Methods: Eighty-one participants who ingested or otherwise were exposed to
a deer with chronic wasting disease at a local New York State sportsman's feast
were recruited for this study. Participants were administered an exposure
questionnaire and agreed to follow-up health evaluations longitudinally over the
next six years.
Results: Our results indicate two types of risks for those who attended the
feast, a Feast Risk and a General Risk. The larger the number of risk factors,
the greater the risk to human health if CWD is transmissible to humans.
Long-term surveillance of feast participants exposed to CWD is ongoing.
Conclusion: The risk data from this study provide a relative scale for
cumulative exposure to CWD-infected tissues and surfaces, and those in the upper
tiers of cumulative risk may be most at risk if CWD is transmissible to humans.
Background
Chronic Wasting Disease (CWD) was first observed in the United States in
the late 1960s, though its origins are still unclear [1,2]. The term "chronic
wasting disease" was first used in 1967 to describe clinical symptoms in captive
Colorado mule deer [1,2]. In 1978, the disease was diagnosed as a spongiform
encephalopathy [1,3]. By 1980, CWD had been described in captive elk and mule
deer herds in both Colorado and Wyoming [1,2]. Subsequently in 1985, CWD was
found in free-ranging elk in Wyoming, and recognized in free-ranging mule deer
and whitetail deer in both states by 1990 [3]. CWD has since been described in
14 states across the US and in 2 provinces in Canada (Figure 1).
In April of 2002, the New York State Department of Environmental
Conservation (NYSDEC) began a statewide surveillance program for CWD in
whitetail deer [4]. The first positive samples (five in total) were confirmed in
April 2005 from animals on two domestic deer farms in Oneida County, NY. The
second deer farm, located very near to the first, received two deer that tested
positive from the first deer farm. In response, the NYSDEC implemented an
intensive mandatory surveillance of CWD, primarily in Oneida and Madison
counties [4]. In order to monitor the wild deer herd, a CWD containment area was
created encompassing approximately a 10 mile radius around the location of the
CWD positive domestic deer farms in Oneida and Madison counties (Figure 1) [4].
During the initial phase of intensive monitoring (through April 30, 2005), 317
wild deer were collected and tested from this containment area as well as from
the Town of Arietta in Hamilton County. Wild deer (two in total), in close
proximity to the domestic deer farms, were found to be positive for CWD. During
the second phase of the intensive monitoring program, all deer that died or were
killed within this area were subject to mandatory testing (Figure 2).
Additionally, the NYSDEC expanded its testing program statewide [4], and now the
annual testing of deer for CWD includes 800–1000 animals within the containment
area (Figure 1) and approximately 5000 animals statewide [4]. No additional
positive deer, wild or domestic, have been found since April 2005. Details of
the distribution of the deer tested across New York State for CWD can be found
on the DEC website [4].
Traditions of hunting deer, elk, moose, and other cervids, and management
of domestic cervid preserves bring humans into contact with animals that could
have CWD. Currently, it is unclear whether CWD prions can be naturally
transmitted from infected cervids to humans or to non-cervids. The question of
cross-species transmission of CWD has been raised in the past [5-13]. In 2002 an
unusual cluster of Creutzfeldt-Jakob Disease (CJD) – a human prion disease –
developed in individuals who were avid lifelong Idaho deer hunters [14];
however, this and other reports investigating clusters of CJD have failed to
establish a link with exposure to cervids through hunting or consuming the
animals, or through other associated behaviors [12,14-18]. Although still
unclear for CWD, epidemiological and laboratory findings have established an
unequivocal link between Bovine Spongiform Encephalopathy (BSE) and vCJD
[11,19-26].
On March 13, 2005, a local fire company in Oneida County, New York, hosted
approximately 200–250 individuals at their annual Sportsmen's Feast, during
which local wild game, including venison (deer meat), was prepared, cooked in
various ways, served, and consumed by individuals primarily from Oneida and
neighboring counties. Shortly thereafter, laboratory tests indicated that one of
the deer served was positive for CWD [27]. Since 2002, the New York State
Department of Environmental Conservation has required the mandatory testing of
deer for CWD harvested from a domestic deer farm. However, there is no
requirement that the meat not be consumed before the results are made available
and thus reaction to the finding that the deer tested positive ranged from
unconcerned to anger. Feast attendees were exposed to the contaminated meat
through a variety of activities, including butchering and processing, cooking,
consumption of venison, and/or through contact with contaminated surfaces. This
incident represents the only known large scale point-source exposure of humans
to an animal with confirmed CWD.
In response to this known point-source exposure, the Oneida County Health
Department and the State University of New York at Binghamton (SUNY) proposed
and launched the Oneida County Chronic Wasting Disease Surveillance Project, a
cohort study designed to examine a natural experimental model of human exposure
to CWD. The objective of the study are to determine the potential human health
risks associated with exposure to CWDcontaminated cervids by following the
events and health outcomes of attendees at the Sportsmen's Feast. Study
participants are being followed for a minimum period of six years from the time
of exposure. This is based on the minimum incubation period and earliest age at
onset for known human prion diseases including vCJD [11] and kuru [28-31]. The
current report describes the initial results of a risk analysis based on
behaviors associated with the wild game feast in upstate New York.
snip...
General Risk
Results regarding General Risk factors are presented in Figure 5. In
relation to deer hunting practices, of the 81 participants, 69.1% hunted deer,
and of those who hunted, 80.4% harvested a deer between the years 2000–2005. Of
those who hunted, 25.0% reported hunting only in Oneida County. Furthermore, a
total of 32.1% of the participants indicated that they hunted in the Oneida
County CWD containment area, although not exclusively. Of those who hunted,
96.4% field dressed, 75.5% removed antlers and 70.9% butchered harvested deer.
However, only 26.4% of them wore gloves while butchering deer. Of those who
hunted, 92.7% consumed the deer they killed, and 96.3% of all feast participants
reported eating venison outside of the Sportsmen's Feast. Of the 81
participants, 24.6% also reported eating venison from other states. In addition
to hunting, the 81 participants reported general contact with animals, including
deer (39.5%), cattle (13.6%), sheep (1.2%), alpacas (1.2%), and other animals
(9.9%).
Discussion
The purpose of this report is to describe the events surrounding the
exposure of a large cohort of individuals to a CWD-infected animal, and present
information on risk behaviors for activities at the feast and general hunting
behaviors outside the feast. This study focuses on two levels of risk, that
specific to activities at the feast, Feast Risk, and activities outside the
feast, General Risk. Because CWD has not been definitively linked to the
development of a prion disease in humans, the risk behaviors evaluated reflect
those associated with known prion disease transmission routes
[11,19-26,28-33].
Studies have shown that CWD can be experimentally transmitted to voles
[13], non-human primates [7], cattle [5,8], and sheep [9]. Since transmissible
spongiform encephalopathies have the ability to cross species barriers and are
resistant to degradation [5-10,13,16,18,28,29,32- 34], food chain transmission
of prion diseases is a growing human and animal health concern. Infected prions
are found in the blood, skeletal muscle, and saliva as well as the central
nervous system of infected animals [5,10,33,35]. Contact with these tissues is a
likely mode of transmission of CWD from animal to animal, and could potentially
present a risk to humans. It is currently considered unlikely that CWD can cross
the species barrier to humans [12,14,18]. However, if it can, those with
multiple risk factors may be most vulnerable. The information presented above
provides a relative scale for cumulative exposures to CWD-infected tissues and
surfaces.
Since CWD has spread from regions of the Midwest with generally low human
population densities to high-density regions of the Eastern U.S. (New York and
West Virginia), direct contact between infected cervids and humans has
increased. Additionally, the potential for cross-species transmission of CWD
from deer to cattle to humans may be increased as a result of increasing contact
between large herds of potentially infected cervids and cattle in pastures on
smaller Eastern U.S. farms.
Conclusion
The Oneida County CWD Surveillance Project introduced here, and the data
reported in this paper, provides the first step in developing a natural
experimental model of possible transmission of CWD prions from deer to humans
[36,37] with a known point-source exposure. Surveillance of the cohort will
continue for a minimum of six years (and likely extended) through annual
follow-up questionnaires including self-report health information. Since human
prion diseases are reportable in New York State, the Oneida County Health
Department and health departments in other neighboring counties will be
especially vigilant in this surveillance effort. This prospective cohort study
will provide new information previously unavailable from retrospective studies
where the CWD status of cervids was unknown and hunting behaviors only evaluated
retrospectively many years after onset of cases of CJD.
February 21, 2003 / 52(07);125-127
Fatal Degenerative Neurologic Illnesses in Men Who Participated in Wild
Game Feasts --- Wisconsin, 2002
Creutzfeldt-Jakob disease (CJD) is a fatal neurologic disorder in humans.
CJD is one of a group of conditions known as transmissible spongiform
encephalopathies (TSEs), or prion diseases, that are believed to be caused by
abnormally configured, host-encoded prion proteins that accumulate in the
central nervous tissue (1). CJD has an annual incidence of approximately 1 case
per million population in the United States (1) and occurs in three forms:
sporadic, genetically determined, and acquired by infection. In the latter form,
the incubation period is measured typically in years. Recent evidence that prion
infection can cross the species barrier between humans and cattle has raised
increasing public health concerns about the possible transmission to humans of a
TSE among deer and elk known as chronic wasting disease (CWD) (2). During
1993--1999, three men who participated in wild game feasts in northern Wisconsin
died of degenerative neurologic illnesses. This report documents the
investigation of these deaths, which was initiated in August 2002 and which
confirmed the death of only one person from CJD. Although no association between
CWD and CJD was found, continued surveillance of both diseases remains important
to assess the possible risk for CWD transmission to humans.
Case Reports
Case 1. In December 1992, a Wisconsin man aged 66 years with a history of
seizures since 1969 sought treatment for recurring seizures, increasing
forgetfulness, and worsening hand tremors. Electroencephalographic (EEG)
examination demonstrated focal epileptiform activity and nonspecific diffuse
abnormalities, but no specific diagnosis was made. In February 1993, he was
hospitalized for increasing confusion, ataxia, and movement tremors of his
extremities. A magnetic resonance image (MRI) demonstrated mild, nonspecific
enhancement along the inferior parasagittal occipital lobe. A repeat EEG showed
bifrontal intermittent, short-interval, periodic sharp waves, suggesting a
progressive encephalopathy; a diagnosis of CJD was suspected. The man died later
that month; neuropathologic examination of brain tissue during autopsy indicated
subacute spongiform encephalopathy, compatible with CJD.
The man was a lifelong hunter who ate venison frequently. He hunted
primarily in northern Wisconsin but also at least once in Montana. He hosted
wild game feasts at his cabin in northern Wisconsin from 1976 until shortly
before his death. Fixed brain tissue obtained during the autopsy was sent for
analysis to the National Prion Disease Pathology Surveillance Center (NPDPSC)
and reexamined at the institution where the autopsy was conducted.
Histopathologic examination did not substantiate the diagnosis of prion disease.
In addition, 27 brain tissue sections were negative for prions by immunostaining
despite positive antibody reactions against other proteins (controls), which
indicated that other epitopes in the tissue samples were preserved.
Case 2. In May 1999, a Minnesota man aged 55 years with no previous history
of a neurologic disease sought evaluation and treatment following a 3-month
history of progressive difficulty in writing and unsteadiness of gait. A
computerized tomography (CT) scan and MRI examination of his head did not
indicate any abnormality. In June 1999, he was hospitalized following onset of
dementia, speech abnormalities, and myoclonic jerking. An EEG indicated
left-hemispheric periodic sharp waves and moderate generalized background
slowing; CJD was diagnosed clinically. In July 1999, following worsening
symptoms and development of right upper extremity dystonia, the patient died.
Neuropathologic evaluation of brain tissue during autopsy demonstrated
widespread subcortical spongiform lesions, consistent with CJD.
The man was not a hunter but had a history of eating venison. He made an
estimated 12 visits to the cabin where the wild game feasts were held, but he
participated in only one feast during the mid-1980s. Sections of fixed and
frozen brain tissue obtained during autopsy were analyzed at NPDPSC, and prion
disease was confirmed by immunohistochemical and Western blot testing. The
Western blot characteristics and prion disease phenotype in this patient were
consistent with the most common form of sporadic CJD, classified as M/M (M/V) 1
(3). Subsequent genetic typing confirmed the presence of methionine homozygosity
(M/M) at codon 129 of the patient's prion protein gene.
Case 3. In June 1992, a Wisconsin man aged 65 years sought treatment for
progressive slowing of speech, worsening memory, and personality changes. By
January 1993, his speech was reduced to one-word utterances. Neurologic
examination showed a flat affect, decreased reflexes, and apraxia. A CT head
scan showed mild atrophy, and an EEG was normal. Pick's disease was diagnosed.
By May, he was unable to perform any daily living activities; he died in August
1993. Neuropathologic evaluation of brain tissue during autopsy showed
symmetrical frontal lobe cerebral cortical atrophy and mild temporal lobe
atrophy. No Pick's bodies or spongiform lesions were observed.
The man had a history of eating venison and participated regularly in wild
game feasts held at the cabin owned by patient 1. He was a lifelong hunter and
hunted mostly in Wisconsin but also in Wyoming and British Columbia. No game was
brought to the wild game feasts from his hunting trips outside of Wisconsin.
Examination of fixed brain tissue sent to NPDPSC demonstrated no lesions
indicative of CJD, and immunohistochemical testing with antibody to the prion
protein did not demonstrate the granular deposits seen in prion diseases.
Epidemiologic Investigation
Wild game feasts consisting of elk, deer, antelope, and other game that
occurred at a cabin in northern Wisconsin owned by patient 1 began in 1976 and
continued through 2002. These feasts typically involved 10--15 participants and
usually occurred on weekends before or during hunting seasons in the fall and
occasionally in the spring. Wild game brought to these feasts usually were
harvested in Wisconsin, but three men who attended these feasts reported hunting
in the western United States and bringing game back to Wisconsin. These
activities took place in Colorado (near the towns of Cortez, Trinidad, Collbran,
Durango, and Meeker), Wyoming (near the towns of Gilette and Cody), and Montana
(near the town of Malta). CWD was not known to be endemic in these areas at the
time that these hunting activities took place.
Information was obtained for 45 (85%) of 53 persons who were identified as
possibly participating in the wild game feasts; all were male. Information was
obtained by direct interview or from family members of decedents. Of the 45
persons, for whom information was obtained, 34 were reported to have attended
wild game feasts. Seven of the 34 feast attendees were deceased, including the
three patients. None of the four other decedents had a cause of death attributed
to or associated with a degenerative neurologic disorder. None of the living
participants had any signs or symptoms consistent with a degenerative neurologic
disorder.
Reported by: JP Davis, MD, J Kazmierczak, DVM, M Wegner, MD, R Wierzba, Div
of Public Health, State of Wisconsin Dept of Health and Family Svcs. P Gambetti,
National Prion Disease Pathology Surveillance Center, Case Western Reserve
University, Cleveland, Ohio. L Schonberger, MD, R Maddox, MPH, E Belay, MD, Div
of Viral and Rickettsial Diseases, National Center for Infectious Diseases; V
Hsu, MD, EIS Officer, CDC.
Editorial Note:
CWD was first described in the United States in the 1960s and classified as
a TSE in 1978. Previously localized to a contiguous endemic area in northeastern
Colorado and southeast Wyoming, since 2000, CWD has been found in free-ranging
deer or elk in Illinois, Nebraska, New Mexico, South Dakota, Wisconsin, and
outside the previously known endemic areas of Colorado and Wyoming. CWD has been
identified also in captive deer or elk in Colorado, Kansas, Minnesota, Montana,
Nebraska, Oklahoma, South Dakota, and Wisconsin (4). Because a variant form of
CJD, with specific neuropathologic and molecular characteristics that
distinguish it from sporadic CJD, has been associated with eating cattle
products infected with a prion that causes bovine spongiform encephalopathy (5),
concern has been raised about the possibility that the prion associated with CWD
might be transmitted to humans in a similar way.
In this investigation, because only one of the three cases in Wisconsin had
neuropathologic confirmation of a prion disease, no association could be made
between case participation in the wild game feasts and the development of CJD.
Although patient 2 had confirmed CJD, he was unlikely to have eaten CWD-infected
venison at these feasts because venison and other game from outside Wisconsin
that was served at these feasts did not originate from known CWD-endemic areas,
and the man participated in the feasts only once. In addition, the prion disease
in this case was consistent with the most common form of sporadic CJD, without
apparent unusual neuropathologic or molecular characteristics that might occur
if the prion related to CWD had been responsible for the disease.
The findings in this report are subject to at least two limitations. First,
not all members participating in wild game feasts could be identified, and not
all persons listed as participating could be contacted for interviews. Second,
interviews that were conducted required recall of events that occurred up to 25
years ago, limiting the detail or accuracy of events. However, the similar
responses obtained from different sources support the accuracy of the
investigation findings.
A previous investigation of unusually young CJD patients in whom the
transmission of CWD was suspected also did not provide convincing evidence for a
causal relationship between CWD and CJD (2). However, limited epidemiologic
investigations cannot rule out the possibility that CWD might play a role in
causing human illness. Ongoing surveillance of CJD, particularly in states with
CWD, is important to assess the risk, if any, for CWD transmission to humans.
Because the confirmation of CJD and the detection of a new prion disease require
neuropathologic study of brain tissue, physicians are encouraged to contact
NPDPSC (http://www.cjdsurveillance.com;
telephone, 216-368-0587) to confirm diagnoses of CJD and to distinguish its
various subtypes. Because of the known severity of TSEs in humans and the
possibility that the CWD prion can affect humans, animals with evidence of CWD
should be excluded from the human food or animal feed chains. Hunters and wild
venison consumers should follow precautionary guidelines available from the
Wisconsin Department of Agriculture, Trade, and Consumer Protection (http://datcp.state.wi.us/core/consumerinfo)
to prevent potential exposures to the CWD agent.
References
PLEASE NOTE ;
*** In some cases, the incubation period may be as long as 50 years
At a hearing in Parliament last Wednesday, the Science and Technology
Committee was told that vCJD continued to pose a “significant” risk to UK public
health and that more than one in every 2000 people could be silent carriers of
the disease. *** vCJD can have an incubation period of over 30 years.
Monday, February 03, 2014
CREUTZFELDT-JAKOB DISEASE T.S.E. PRION U.K. UPDATE As at 3rd February 2014
*** Because typical clinical signs of BSE cannot always be observed in
nonambulatory disabled cattle, and because evidence has indicated these cattle
are more likely to have BSE than apparently healthy cattle, FDA is designating
material from nonambulatory disabled cattle as prohibited cattle materials.
***In addition, non-human primates are specifically susceptible for
atypical BSE as demonstrated by an approximately 50% shortened incubation time
for L-type BSE as compared to C-type. Considering the current scientific
information available, it cannot be assumed that these different BSE types pose
the same human health risks as C-type BSE or that these risks are mitigated by
the same protective measures.
Hence, the data presented here are important for a risk- based SRM
definition.
Competing interests
The authors declare that they have no competing interests.
see much more here ;
Saturday, December 21, 2013
Complementary studies detecting classical bovine spongiform encephalopathy
infectivity in jejunum, ileum and ileocaecal junction in incubating cattle
From: TSS
Subject: CWD--THE FEAST--Investigators find no common source in hunters'
deaths $$$ (or did they???)
Date: November 22, 2002 at 6:22 am PST
Investigators find no common source in hunters' deaths 2 of 3 show absence
of prions
By JOHN FAUBER and LEE BERGQUIST jfauber@journalsentinel.com Last Updated:
Nov. 21, 2002
Three hunters who ate wild game together and later died of rare brain
disorders did not contract their diseases from a common source such as venison,
a four-month-long investigation concluded Thursday. [19335] Chronic Wasting
Disease For complete archived coverage of chronic wasting disease in Wisconsin,
go to our SPECIAL SECTION Quotable The idea here is that there is no fear now.
These cases are one of the things that stopped many spouses, or hunters from
hunting, because it sounded so plausible - and now it is completely debunked. -
Fred Bannister, Chetek physician who attended many game dinners with the late
Wayne Waterhouse Related Coverage Deer hunting: Season starts saturday Section:
Outdoors Section: Chronic wasting disease
A report by federal and state health investigators found that one of the
men apparently had been misdiagnosed with Creutzfeldt-Jakob disease, a
neurological disorder caused by prions. Prions are the same unusual infectious
agents that cause chronic wasting disease in deer and elk.
Pathologists were able to run new tests of brain tissue from Wayne
Waterhouse of Chetek, who died in 1993, and determined that there was no
evidence of a prion-related illness, said Jeffrey Davis, the state
epidemiologist for communicable diseases.
Health officials said they did not know what brain disorder killed
Waterhouse, an avid hunter and outdoorsman.
In September, health officials said new test results from brain tissue
samples of another man, Roger Marten of Mondovi, also showed no evidence of
prions or Creutzfeldt-Jakob disease. A third man, James Botts of Minneapolis,
did die of the disease, the new analysis of his tissue confirmed.
"These results are important because if all three men had developed a rare
disease like CJD (Creutzfeldt-Jakob disease), such a cluster would suggest a
common source of exposure," Davis said. "Thanks to a new testing process not
available at the time of the initial diagnosis of CJD in these patients, we were
able to demonstrate the absence of prions in brain tissues of two of the
patients."
The new analysis, part of a joint investigation by the Wisconsin Division
of Health and the U.S. Centers for Disease Control and Prevention, contradicts a
1993 diagnosis made at the Mayo Clinic, where Waterhouse died.
The new report could buoy the confidence of deer hunters. The report was
issued two days before the start of the 2002 gun deer season.
The hunt is considered the most important in decades because of a plan by
the state Department of Natural Resources to eradicate 25,000 deer in a
411-square-mile region of Dane, Iowa and Sauk counties to control the spread of
chronic wasting disease.
The disease has prompted questions about the safety of venison and has
helped drive down the number of deer hunters buying licenses this year.
"From a hunters' standpoint, (the report) may give hunters a little more
confidence about consuming venison," said Darrell Bazzell, secretary of the
DNR.
Sales of deer-hunting licenses have picked up in the past few weeks, but as
of Wednesday sales lagged 16% behind the same time last year, according to the
DNR. So far this year, there have been 118,441 fewer licenses sold.
Bazzell said the new findings could give an additional last-minute boost to
license sales.
Thursday's report contradicts the findings of a Mayo Clinic doctor, who in
a May 17, 1993, letter to Waterhouse's family said a postmortem exam of
Waterhouse confirmed that he died of Creutzfeldt-Jakob disease.
In fact, when reached at home on Thursday night, Joseph Parisi, a Mayo
pathologist, said the new tests on Waterhouse were "inconclusive" and could not
confirm that he died of the disease.
That differs from a statement issued Thursday by Davis' office, which says
that Waterhouse did not have Creutzfeldt-Jakob disease. Davis also said the
latest analysis was confirmed by pathologists at the National Prion Disease
Pathology Surveillance Center in Cleveland.
The center receives federal funding to monitor prion diseases, including
the human version of mad cow disease, and is considered one of the top prion
labs in the country.
Davis said it was his understanding that pathologists at the lab concurred
with pathologists at Mayo and also were in agreement on the new analysis of
Waterhouse's tissue.
The case of the three outdoorsmen was first reported in the Journal
Sentinel in July and has since attracted widespread attention and heightened
concerns about the safety of venison.
Waterhouse, Marten and Botts, a former Chetek resident who later moved to
Minneapolis, all had eaten wild game at the Waterhouse family cabin on the Brule
River in northern Wisconsin.
Chetek physician Fred Bannister, who attended many of the game dinners with
Waterhouse, emphasized that no deer from the dinners came from the
411-square-mile eradication zone.
Bannister, also a deer hunter, said he had been waiting for scientific
corroboration that his friend had not died of Creutzfeld-Jacob disease.
"How can you have good news about someone who died?" Bannister said. "But
the idea here is that there is no fear now. These cases are one of the things
that stopped many spouses, or hunters from hunting, because it sounded so
plausible - and now it is completely debunked."
However, Judy Botts, wife of James Botts, said the new findings had not
changed her mind.
Botts still suspects that her husband's consumption of venison played a
role in his death, "but it can't be proven," she said. "I knew it all
along."
Botts died in 1999. New analysis of his tissue confirmed his diagnosis of
Creutzfeldt-Jakob disease, which occurs at the annual rate of about one per
million people.
Marten died in 1993. He initially was diagnosed with Pick's disease,
another rare brain disease. A new analysis of his brain tissue found that
although he did have Pick's, he did not have a prion disease.
About 75 men were known to attend the wild game feasts, Davis said.
Investigators have been able to contact about 45 of them. No other case of rare
brain disease has been found.
Davis said the new findings were consistent with earlier statements by
health organizations that chronic wasting disease prion "has not been shown to
cause human illness."
Some neurologists and prion researchers have cautioned that the question of
whether chronic wasting disease can jump to people remains unanswered.
Some have said that until proved otherwise, it is reasonable to assume that
the disease may jump to people in a manner similar to mad cow disease. Mad cow
disease is believed to have caused at least 130 cases of
variant-Creutzfeldt-Jakob disease, an always fatal disorder, in about 130
people, mainly in Great Britain.
The new information could entice some wavering hunters to head into the
woods, said David Ladd, chairman of the Big Game Committee of the Conservation
Congress, a citizens group that advises the DNR.
But Ladd said the discovery of chronic wasting disease had altered the
psyche of the 2002 hunt.
"A lot of hunters are probably not going to make a decision until they pull
the trigger," he said.
A version of this story appeared in the Milwaukee Journal Sentinel on Nov.
22, 2002.
HMMM???????
SNIP...
Thursday's report contradicts the findings of a Mayo Clinic doctor, who in
a May 17, 1993, letter to Waterhouse's family said a postmortem exam of
Waterhouse confirmed that he died of Creutzfeldt-Jakob disease.
In fact, when reached at home on Thursday night, Joseph Parisi, a Mayo
pathologist, said the new tests on Waterhouse were "inconclusive" and could not
confirm that he died of the disease.
That differs from a statement issued Thursday by Davis' office, which says
that Waterhouse did not have Creutzfeldt-Jakob disease. Davis also said the
latest analysis was confirmed by pathologists at the National Prion Disease
Pathology Surveillance Center in Cleveland.
The center receives federal funding to monitor prion diseases, including
the human version of mad cow disease, and is considered one of the top prion
labs in the country.
SNIP...
$$$
TSS
11/21/02, LAB FINDINGS RELEASED ON FATAL CASES OF NEUROLOGIC DISEASES IN
OUTDOORSMEN
Contact: Jeffrey P. Davis, M.D. (608) 267-9003 James Kazmierczak, DVM (608)
266-2154 CDC Press Office (404) 639-3286
FOR IMMEDIATE RELEASE
(MADISON ? November 21, 2002) -- The Wisconsin Division of Public Health
today released completed test results related to the investigation into the
fatal cases of degenerative neurological illnesses in three men who consumed
wild game served during a series of feasts.
The test results announced today indicate that Wayne Waterhouse, a northern
Wisconsin resident who died in 1993, did not have Creutzfeldt-Jakob disease
(CJD) or any other evidence of prions or prion-related illness. Results already
made public indicated that another of the patients, Roger Marten, a northern
Wisconsin resident who died in 1993, also did not have CJD or any other evidence
of prions or prion-related illness. Only one of the three men, James Botts, a
Minnesota resident who died in 1999, had a confirmed diagnosis of CJD.
"These results are important because if all three men had developed a rare
disease like CJD, such a cluster would suggest a common source of exposure,"
said Dr. Jeffrey Davis, Wisconsin State Epidemiologist for Communicable
Diseases, in reporting the findings. "Thanks to a new testing process not
available at the time of the initial diagnosis of CJD in these patients, we are
able to demonstrate the absence of prions in the brain tissues of two of the
patients. Therefore, these three cases cannot be attributed to a common source
of illness."
The current investigation, conducted by the Division of Public Health and
the U.S. Centers for Disease Control and Prevention, was initiated after reports
surfaced that rare degenerative neurological diseases had occurred in three
acquaintances who shared meals of wild game in northern Wisconsin. The reports
generated considerable public interest due to the concern that these illnesses
might somehow be linked to chronic wasting disease (CWD) of deer and elk.
"These findings are consistent with earlier statements by the CDC and the
World Health Organization that the CWD prion has not been shown to cause human
illness," Dr. Davis added. "They also illustrate the ongoing need to apply the
most current scientific techniques to the important issue of understanding CWD
and other prion-related conditions."
Specimens of brain tissue from each of the three men had been collected
during the individuals? autopsies. The tissues were recently forwarded to the
National Prion Disease Pathology Surveillance Center in Cleveland, Ohio, where
pathologists examined the specimens for evidence of CJD and the presence of
abnormal prion proteins which cause the illness. This pathology center was
established during 1996-1997 by CDC in collaboration with the American
Association of Neuropathologists to enable state-of-the-art laboratory
investigation of physician-diagnosed and suspected cases of prion disease in the
United States.
Creutzfeldt-Jakob disease is a fatal degenerative brain condition of humans
believed to be caused by an abnormally-shaped protein called a prion. It occurs
at a rate of about one case per million people per year throughout much of the
world, and was first described in the 1920s. Chronic wasting disease in deer and
elk is also believed to be caused by a prion and produces lesions in the brain,
but the deer CWD prion has not been shown to affect humans.
Dr. Davis reiterated that while these new results are reassuring, it is
still impossible to say with absolute certainty that the CWD prion will never
cause human illness. As a precaution, he continues to advise that hunters
process their venison in a safe manner and not ingest tissues where the CWD
prion is known to concentrate. These tissues include brain, spinal cord, eyes,
lymph nodes and spleen. The Wisconsin Department of Agriculture, Trade, and
Consumer Protection has issued recommendations on processing deer. These can be
found on their website at http://datcp.state.wi.us/ah/agriculture/animals/disease/chronic/pdf/venison_safety_2side.pdf
.
-30-
Last Revised: November 21, 2002
Date: Fri, 22 Nov 2002 14:14:12 –0600
Reply-To: Bovine Spongiform Encephalopathy Sender: Bovine Spongiform
Encephalopathy
From: "Terry S. Singeltary Sr."
Subject: Re: Investigators find no common source in hunters' deaths $$$ (or
did they???)
######## Bovine Spongiform Encephalopathy #########
greetings list members,
"jimmeny cricket" !!!
how about a statement from Gambetti et al, instead of a bunch of alleged
second hand statements.
does state epidemiologist or even mayo really have access to a specialized
panel of _proven_ antibodies and know how with prion ihc??? probably not.
only gambetti and prusiner have the necessary reference collections if i am
not mistaken $$$
who validated it, false positive, false negatives?
what's going on here???
just in time too to avert a public panic and at the opening weekend of deer
hunting season at that, how convenient and excellent timing$$$
unpublished, unpeer-reviewed = unreliable
and just more BSeee.
SNIP...
THE FEAST WISCONSIS
Wednesday, November 16, 2011
Wisconsin Creutzfeldt Jakob Disease, CWD, TSE, PRION REPORTING 2011
Q93. If Chronic Wasting Disease was found in an area where you deer hunt in
Maryland and regulations were implemented to prohibit the removal of whole deer
carcasses from the area, do you agree or disagree that you would stop deer
hunting in that area?
Strongly agree
20 26 33 32
Percent who strongly or moderately agree they would stop deer hunting given
the following conditions.
30 39 49 44
Q93. If Chronic Wasting Disease was found in an area where you deer hunt in
Maryland and regulations were implemented to prohibit the removal of whole deer
carcasses from the area
Hunters’ Attitudes Toward CWD and Management Efforts in Hampshire County 65
Note: Graph shows results obtained from seven questions. Each item was asked
about individually.
14
28
28
27
27
27
19
0 20 40 60 80 100
Q87. The presence of Chronic Wasting Disease in Hampshire County
Q91. The ban on baiting and feeding deer in Hampshire County
Q88. Because you are concerned the deer you harvest or the meat you consume
might be infected with Chronic Wasting Disease
Q92. The carcass transportation restrictions for Hampshire County
Q89. Because you feel you cannot be sure the deer you harvest in Hampshire
County is not infected with Chronic Wasting Disease
Q90. Because you are concerned you might get Chronic Wasting Disease from
deer in Hampshire County
Q93. The presence of the West Virginia Division of Natural Resources at
checking stations in Hampshire County Percent (n=259)
Percent who indicated that the following strongly or moderately influenced
their decision to deer hunt less or stop deer hunting in Hampshire County since
2004. (Among those whose deer hunting participation in Hampshire County since
2004 decreased or stopped.)
THESIS HUNTERS’ RESPONSE TO CHRONIC WASTING DISEASE IN FOUR STATES
Submitted by Katie M. Lyon Department of Human Dimensions of Natural
Resources In partial fulfillment of the requirements For the Degree of Master of
Science Colorado State University Fort Collins, Colorado Spring 2011
snip...
Results
Bivariate analysis
Across the entire sample, 27% of respondents indicated that they would stop
hunting because of CWD (Table I). All five independent variables were
statistically significant predictors of stopping hunting in the state and thus
provide evidence to support the first hypothesis. The greater the prevalence of
CWD in the state the more likely hunters were to quit. At the lowest
hypothetical prevalence level, 13% indicated that they would no longer hunt in
the state. When prevalence reached 50% statewide, 52% said that they would stop
hunting. The difference in these distributions was statistically significant (χ2
= 3,338.46, p < .001, r = .37).
If CWD were to cause human death, respondents were significantly more
likely to stop hunting in the state (χ2 = 1,187.99, p < .001, r = .25).
Forty-three percent indicated that they would quit hunting in the hypothetical
scenarios where a hunter had died due to CWD; only 19% said they would stop in
the “no human death” scenarios. When hunters’ perceived extreme risks associated
with CWD, 46% would stop hunting in the state. By comparison, 19% would quit
hunting when they perceived no CWD related risks (χ2 = 600.27, p < .001, r =
.17).
Whether or not CWD had been detected in the state and the respondents’
state of residency were also significant predictors of hunters’ behavioral
intentions. Individuals who had hunted in states that did not have CWD were
slightly more likely (30%) to stop hunting than those who had hunted in a CWD
state (25%). Nonresidents (29%) were slightly more likely to quit than residents
(24%). These relationships, however, were not strong for either the presence of
CWD in a state or residency (r = -.05 in both cases).
snip...
The significant 3-way interaction quit hunting * perceived risk * resident,
for example, indicated that nonresidents of the state who perceived greater risk
were more likely to quit hunting deer in the state. In the 4-way interaction,
stopping hunting increased: (a) when prevalence increased, (b) a human death
attributable to CWD had occurred, and (c) if CWD had been detected in the state.
Under the worst case scenario (i.e., 50% prevalence statewide, human death, a
non-CWD state), 64% of the respondents would stop hunting in the state (Table
3.3). If the prevalence of CWD was 50% statewide, a human death had occurred,
and the disease had been detected in the state, 60% would quit hunting.
Consistent with past research, if CWD is concentrated in a single area at
relatively low prevalence levels, few hunters would quit the activity.
snip...
Interactions among the predictors were hypothesized to increase the
potential for stopping hunting in the state. Multivariate analysis confirmed
that the decision to stop hunting interacted with all five predictors and
suggested that combinations of these predictors increase the probability of
quitting. The 4-way interaction, for example, revealed that 60% or more of our
respondents would stop hunting if CWD prevalence ever reached 50% statewide and
a human death attributable to CWD had occurred. These findings support our
second hypothesis and have implications for management, theory, and
research.
Human Dimensions of Wildlife, 9:211–231, 2004 Copyright © Taylor &
Francis Inc. ISSN: 1087–1209 print / 1533-158X online DOI:
10.1080/10871200490479990
Hunters’ Behavior and Acceptance of Management Actions Related to Chronic
Wasting Disease in Eight States
MARK D. NEEDHAM JERRY J. VASKE MICHAEL J. MANFREDO Department of Natural
Resource Recreation and Tourism Human Dimensions in Natural Resources Unit
Colorado State University Fort Collins, Colorado, USA
The impacts of chronic wasting disease (CWD) on hunters’ behavior and
beliefs about acceptable management actions are not clearly understood. This
article presents findings from an initial phase of a multi-stage, multi-state
effort to address these knowledge gaps. Data were obtained from mail surveys (n
= 659) of resident and nonresident deer hunters in eight states and elk hunters
in three states. Hunters were presented with hypothetical situations of
increasing:
(1) CWD prevalence (all eight states), and
(2) human health risks (two states).
Logistic regression equations estimated that at current prevalence levels
in some states, 3% (residents) to 5% (nonresidents) of hunters would stop
hunting deer/elk in their state.
If 50% of the deer or elk across the state were infected, approximately 42%
(residents) and 54% (nonresidents) would stop hunting deer/elk in their state.
In hypothetical situations where a hunter died from CWD at this prevalence
level, the percentage was 68%.
Potential for conflict indices (PCI) showed that as prevalence and human
health risks increased, acceptability of testing and lethal management increased
and acceptability of allowing CWD to take its natural course decreased.
snip...
Hunters’ Responses to CWD in Eight States 219
Results
Descriptive and Bivariate Findings
In total, 5% of the hunters reported that they would stop hunting deer/elk
in the state if 10% of the deer or elk in zone A and 0% in the rest of the state
(zones B and C) were infected with CWD (Table 1). This prevalence level is
consistent with current conditions in parts of some states (e.g., Colorado,
Wyoming). The percentage of respondents that would stop hunting deer/elk in the
state increased as prevalence and distribution increased. For example, if CWD
prevalence was 50% in zone A, 30% in zone B, and 10% in zone C, 32% of hunters
would stop hunting deer/elk in the state. If 50% of the deer or elk across the
entire state were infected, 49% of hunters reported that they would stop hunting
deer/elk in the state.2 Across all eight states, a similar proportion of
respondents hunted most often in zone A (30%), B (33%), or C (37%) in
2002.
snip...
Results, however, suggest more serious potential ramifications of CWD.
Research has shown that although it is unlikely to occur, CWD can reach higher
prevalence levels in deer and elk populations (Gross & Miller, 2001; Miller
et al., 2000; Williams & Young, 1980) and the potential for human
susceptibility to CWD may exist (Belay et al., 2004; Raymond et al., 2000). If
CWD prevalence among deer or elk ever increases to 50% across a state, 49% of
hunters will stop hunting deer/elk in the state. Based on the findings from
South Dakota and Wisconsin, 60% to 68% of hunters will stop hunting deer/elk in
their state if this Hunters’ Responses to CWD in Eight States 227 prevalence
level exists and CWD is shown to be transmissible to humans or cause human
death. Even at current prevalence levels (e.g., 10%) in parts of some states
(e.g., Colorado, Wyoming), 16% to 20% of hunters will stop hunting deer/ elk in
their state if CWD affects humans or causes human death.
These findings suggest that if CWD prevalence increases dramatically, deer
and/or elk hunting participation will substantially decrease in several states.
If high levels of prevalence are combined with threats to human health, the
decline could be even greater. This could have compounding and catastrophic
effects on revenues for wildlife agencies, financial and logistical support for
wildlife programs, management and control of deer and elk populations, public
support for wildlife agencies and their ability to manage wildlife resources,
the preservation of cultural and family traditions, and the economic viability
of rural communities that are dependent on hunting revenues. Findings also
suggested that nonresident hunters are more likely than residents to stop
hunting deer/elk in the state as CWD conditions worsen. Declining numbers of
nonresidents could significantly reduce agency revenue from license sales
because they often pay much higher fees for hunting licenses. Taken together,
these consequences of a decline in hunting participation due to CWD suggest the
need for agencies and other stakeholders to engage in long-term and proactive
management planning efforts for addressing the disease.
Although most of the CWD conditions manipulated in this study (i.e., high
CWD prevalence, human health risks) are extremely unlikely, increased testing of
harvested deer and elk (i.e., postmortem samples), advancements in lymphoid and
tonsillar biopsy techniques for testing live animals (i.e., antemortem
sampling), and in-vitro laboratory experiments of CWD in human cells may provide
a more realistic assessment of current and future CWD prevalence levels and
possible risks to human health associated with the disease (Raymond et al.,
2000; Sigurdson et al., 1999; Wild, Spraker, Sigurdson, O’Rourke, & Miller,
2002; Wolfe et al., 2002).
snip...
Keywords chronic wasting disease, hunting, risk behavior, wildlife
management, potential for conflict index
This article is based on a project of the Human Dimensions Committee of the
Western Association of Fish and Wildlife Agencies (WAFWA). The authors thank
Chris Burkett (Wyoming Game and Fish Department), Dana Dolsen (Utah Division of
Wildlife Resources), Jacquie Ermer (North Dakota Game and Fish Department),
Larry Gigliotti (South Dakota Department of Game, Fish and Parks), Ty Gray
(Arizona Game and Fish Department), Larry Kruckenberg (Wyoming Game and Fish
Department), Bruce Morrison (Nebraska Game and Parks Commission), Peter Newman
(Colorado State University), Jordan Petchenik (Wisconsin Department of Natural
Resources), Duane Shroufe (Arizona Game and Fish Department), Linda Sikorowski
(Colorado Division of Wildlife), and Tara Teel (Colorado State University) for
their assistance.
Address correspondence to Mark D. Needham, Department of Natural Resource
Recreation and Tourism, Human Dimensions in Natural Resources Unit, Colorado
State University, Fort Collins, Colorado 80523-1480, USA. E-mail:
mneedham@cnr.colostate.edu
CWD STRAINS TO HUMANS ???
*** These results would seem to suggest that CWD does indeed have zoonotic
potential, at least as judged by the compatibility of CWD prions and their human
PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests
that if zoonotic CWD occurred, it would most likely effect those of the PRNP
codon 129-MM genotype and that the PrPres type would be similar to that found in
the most common subtype of sCJD (MM1).
as I said, what if ?
*** our results raise the possibility that CJD cases classified as VV1 may
include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne
infection by type 1 prions from animals, e.g., chronic wasting disease prions in
cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have
been reported (40, 41). The results of the present study emphasize the need for
traceback studies and careful re-examination of the biochemical properties of
sCJD-VV1 prions. ***
===========================================
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
WHAT IF ?
Saturday, April 19, 2014
Exploring the zoonotic potential of animal prion diseases: In vivo and in
vitro approaches
*** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent
*** Here we report that a human prion strain that had adopted the cervid
prion protein (PrP) sequence through passage in cervidized transgenic mice
efficiently infected transgenic mice expressing human PrP,
*** indicating that the species barrier from cervid to humans is prion
strain-dependent and humans can be vulnerable to novel cervid prion strains.
PPo2-27:
Generation of a Novel form of Human PrPSc by Inter-species Transmission of
Cervid Prions
*** Our findings suggest that CWD prions have the capability to infect
humans, and that this ability depends on CWD strain adaptation, implying that
the risk for human health progressively increases with the spread of CWD among
cervids.
PPo2-7:
Biochemical and Biophysical Characterization of Different CWD Isolates
*** The data presented here substantiate and expand previous reports on the
existence of different CWD strains.
Envt.07:
Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free
Ranging White-Tailed Deer Infected with Chronic Wasting Disease
***The presence and seeding activity of PrPTSE in skeletal muscle from
CWD-infected cervids suggests prevention of such tissue in the human diet as a
precautionary measure for food safety, pending on further clarification of
whether CWD may be transmissible to humans.
>>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO
CONVERSION OF THE HUMAN PRION PROTEIN<<<
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
Wednesday, January 01, 2014
Molecular Barriers to Zoonotic Transmission of Prions
*** chronic wasting disease, there was no absolute barrier to conversion of
the human prion protein.
*** Furthermore, the form of human PrPres produced in this in vitro assay
when seeded with CWD, resembles that found in the most common human prion
disease, namely sCJD of the MM1 subtype.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
HD.13: CWD infection in the spleen of humanized transgenic mice
***These results indicate that the CWD prion may have the potential to
infect human peripheral lymphoid tissues.
Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of
the ability of sheep, cattle and deer prion disease isolates to convert normal
human prion protein to its pathological isoform in a cell-free system
***However, they also show that there is no absolute barrier ro conversion of
human prion protein in the case of chronic wasting disease.
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood,
and mother to offspring transmission
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
there is in fact evidence that the potential for cwd transmission to humans
can NOT be ruled out.
I thought your readers and hunters and those that consume the venison,
should have all the scientific facts, personally, I don’t care what you eat, but
if it effects me and my family down the road, it should then concern everyone,
and the potential of iatrogenic transmission of the TSE prion is real i.e.
‘friendly fire’, medical, surgical, dental, blood, tissue, and or products there
from...like deer antler velvet and TSE prions and nutritional supplements there
from, all a potential risk factor that should not be ignored or silenced. ...
the prion gods at the cdc state that there is ;
''no strong evidence''
but let's see exactly what the authors of this cwd to human at the cdc
state ;
now, let’s see what the authors said about this casual link, personal
communications years ago. see where it is stated NO STRONG evidence. so, does
this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD
transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To:
Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached
to your email), we did not say CWD in humans will present like variant CJD.
That assumption would be wrong. I encourage you to read the whole article
and call me if you have questions or need more clarification (phone:
404-639-3091). Also, we do not claim that "no-one has ever been infected with
prion disease from eating venison." Our conclusion stating that we found no
strong evidence of CWD transmission to humans in the article you quoted or in
any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From:
Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
A prion disease of cervids: Chronic wasting disease
Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported
to the Surveillance Center***,
snip...
full text ;
***********CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb***********
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL
REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases
and controls. For both of these meats there was evidence of a trend with
increasing frequency of consumption being associated with increasing risk of
CJD. (not nvCJD, but sporadic CJD...tss)
These associations were largely unchanged when attention was restricted to
pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating
and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to
be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate.
There is no strong evidence that eating veal less than once per year is
associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar
pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK
OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY
OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker
(p = 0.14). When only controls for whom a relative was interviewed are included,
this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another
exposure, the association between veal and CJD remained statistically
significant (p = < 0.05 for all exposures), while the other exposures ceased
to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical
associations between various meats/animal products and INCREASED RISK OF CJD.
When some account was taken of possible confounding, the association between
VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS
STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an
increased risk of CJD, including liver consumption which was associated with an
apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3
studies in relation to this particular dietary factor, the risk of liver
consumption became non-significant with an odds ratio of 1.2 (PERSONAL
COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
Thursday, October 10, 2013
*************CJD REPORT 1994 increased risk for consumption of veal and
venison and lamb**************
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge
Spencers Lane BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third
annual report from the CJD Surveillance Unit. I am sorry that you are
dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the
Department of Health is committed to publishing their reports as soon as they
become available. In the circumstances it is not the practice to circulate the
report for comment since the findings of the report would not be amended. In
future we can ensure that the British Deer Farmers Association receives a copy
of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed
of the results of any research in respect of CJD. This report was entirely the
work of the unit and was produced completely independantly of the the
Department.
The statistical results reqarding the consumption of venison was put into
perspective in the body of the report and was not mentioned at all in the press
release. Media attention regarding this report was low key but gave a realistic
presentation of the statistical findings of the Unit. This approach to
publication was successful in that consumption of venison was highlighted only
once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical
links between CJD and consumption of venison, would increase, and quite possibly
give damaging credence, to the whole issue. From the low key media reports of
which I am aware it seems unlikely that venison consumption will suffer
adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
Wednesday, September 17, 2014
*** Cost benefit analysis of the development and use of ante-mortem tests
for transmissible spongiform encephalopathies ***
BOTTOM LINE $$$
IF YOU TEST, YOU FIND, and the more you test, the more you will find.
HUMANS ARE EXPENDABLE WITH A SLOW, LONG INCUBATING, 100% FATAL DISEASE,
ONCE CLINICAL DISEASE...tss
Wednesday, September 17, 2014
Cervid Health Business Plan Fiscal Years 2014 to 2018 Animal and Plant
Health Inspection Service Veterinary Services
Monday, May 05, 2014
*** Member Country details for listing OIE CWD 2013 against the criteria of
Article 1.2.2., the Code Commission recommends consideration for listing ***
*** We conclude that TSE infectivity is likely to survive burial for long
time periods with minimal loss of infectivity and limited movement from the
original burial site. However PMCA results have shown that there is the
potential for rainwater to elute TSE related material from soil which could lead
to the contamination of a wider area. These experiments reinforce the importance
of risk assessment when disposing of TSE risk materials.
*** The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC)
are shed in urine of infected deer as early as 6 months post inoculation and
throughout the subsequent disease course. Further studies are in progress
refining the real-time urinary prion assay sensitivity and we are examining more
closely the excretion time frame, magnitude, and sample variables in
relationship to inoculation route and prionemia in naturally and experimentally
CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is
likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
see full text and more ;
Monday, June 23, 2014
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
PPo4-4:
Survival and Limited Spread of TSE Infectivity after Burial
Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute
and R(D)SVS; University of Edinburgh; Roslin, Scotland UK
Scrapie and chronic wasting disease probably spread via environmental
routes, and there are also concerns about BSE infection remaining in the
environment after carcass burial or waste 3disposal. In two demonstration
experiments we are determining survival and migration of TSE infectivity when
buried for up to five years, as an uncontained point source or within bovine
heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters
containing either sandy or clay soil. Migration from the boluses is being
assessed from soil cores taken over time. With the exception of a very small
amount of infectivity found 25 cm from the bolus in sandy soil after 12 months,
no other infectivity has been detected up to three years. Secondly, ten bovine
heads were spiked with TSE infected mouse brain and buried in the two soil
types. Pairs of heads have been exhumed annually and assessed for infectivity
within and around them. After one year and after two years, infectivity was
detected in most intracranial samples and in some of the soil samples taken from
immediately surrounding the heads. The infectivity assays for the samples in and
around the heads exhumed at years three and four are underway. These data show
that TSE infectivity can survive burial for long periods but migrates slowly.
Risk assessments should take into account the likely long survival rate when
infected material has been buried.
The authors gratefully acknowledge funding from DEFRA.
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
*** Overall, therefore, it is considered there is a __greater than
negligible risk___ that (nonruminant) animal feed and pet food containing deer
and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In
Animal Feed
EMC 1 Terry S. Singeltary Sr. Vol #: 1
see my full text submission here ;
*** Susceptibility of UK red deer (Cervus alaphus elaphus) to oral BSE
transmission Project Code: M03024 ***
02/08/2011
The project confirmed that U.K red deer are susceptible to both oral and
intra-cerebral inoculation with the cattle BSE agent. Six clinically positive
(from 26-42 months post inoculation) i.c inoculated and one (56 months post
inoculation) orally dosed deer that tested positive for TSE by
immunohistochemistry and Western blotting using several primary antibodies
demonstrated widespread accumulation of disease specific prion protein in the
central nervous system, peripheral nervous system and enteric nervous system but
none in lymphoreticular system. All showed several brain sites positive for
disease specific prion protein and presented immunohistochemistry and Western
blotting phenotypes with similarities to BSE in sheep, goats and cattle but
unlike those seen in chronic wasting disease (CWD) in elk or scrapie in sheep.
The vacuolar pathology and distribution of disease specific prion protein in red
deer resembled that of CWD in most major respects however we have shown that BSE
can be clearly differentiated from CWD by existing immunohistochemical and
biochemical methods that are in routine use.
The knowledge gained as a result of this work will permit rapid and
accurate diagnosis should a TSE ever be detected in European red deer and will
also enable effective disease control methods to be quickly put in place.
Results
We confirmed that U.K red deer are susceptible to both oral and
intra-cerebral inoculation with the cattle BSE agent. Six clinically positive
(from 26-42mpi) i.c inoculated and one (56mpi) orally dosed deer that tested
positive for TSE by IHC and WB using several primary antibodies demonstrated
widespread accumulation of disease specific PrP in CNS, PNS and ENS but none in
LRS. All showed several brain sites positive for disease specific PrP and
presented IHC and WB phenotypes with similarities to BSE in sheep, goats and
cattle but unlike those seen in CWD in elk or scrapie in sheep. The vacuolar
pathology and distribution of PrPd BSE in red deer resembled that of CWD in most
major respects however we have shown that BSE can be clearly differentiated from
CWD by existing immunohistochemical and biochemical methods that are in routine
use.
Final technical report MO3024 01/04/2003 – 31/03/2010 Susceptibility of UK
red deer (Cervus elaphus elaphus) to oral BSE transmission. Stuart Martin - VLA
Lasswade Pentlands Science Park Bush Loan Penicuik EH26 0PZ Page 2 of 21 Further
work undertaken August 2009 – March 2010. Genetic analysis - Wilfred Goldmann;
Roslin NPD.
Negative controls and the remaining 5 orally dosed deer culled at 72mpi
tested negative by IHC and Western blot however analysis of the PrP ORF of these
deer (kindly carried out by Wilfred Goldmann of the Roslin NPD) identified a Q
to E polymorphism at codon 226 that may influence the efficiency of oral
transmission (not published).
In the experimental BSE challenge of red deer six out of six deer succumbed
to BSE when challenged by intracerebral routes but only one of six deer
challenged by the oral route succumbed to infection. Deer killed at 190 days or
365 days post oral challenge showed no evidence of abnormal PrP accumulation
when tested by immunocytochemistry. The PrP gene of red deer includes a Q to E
polymorphism at codon 226. The table shows the distribution of these codon 226
polymorphisms within experimental challenge groups.
snip...
Sunday, December 15, 2013
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
TSS
posted by Terry S. Singeltary Sr. at
11:39 AM
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