Transmission of Chronic Wasting Disease in Wisconsin White-Tailed Deer: Implications for Disease Spread and Management
Transmission of Chronic Wasting Disease in Wisconsin White-Tailed Deer:
Implications for Disease Spread and Management
Christopher S. Jennelle mail,
Viviane Henaux,
Gideon Wasserberg,
Bala Thiagarajan,
Robert E. Rolley,
Michael D. Samuel
Published: March 21, 2014 •DOI: 10.1371/journal.pone.0091043
Abstract
Few studies have evaluated the rate of infection or mode of transmission
for wildlife diseases, and the implications of alternative management
strategies. We used hunter harvest data from 2002 to 2013 to investigate chronic
wasting disease (CWD) infection rate and transmission modes, and address how
alternative management approaches affect disease dynamics in a Wisconsin
white-tailed deer population. Uncertainty regarding demographic impacts of CWD
on cervid populations, human and domestic animal health concerns, and potential
economic consequences underscore the need for strategies to control CWD
distribution and prevalence. Using maximum-likelihood methods to evaluate
alternative multi-state deterministic models of CWD transmission, harvest data
strongly supports a frequency-dependent transmission structure with sex-specific
infection rates that are two times higher in males than females. As
transmissible spongiform encephalopathies are an important and
difficult-to-study class of diseases with major economic and ecological
implications, our work supports the hypothesis of frequency-dependent
transmission in wild deer at a broad spatial scale and indicates that effective
harvest management can be implemented to control CWD prevalence. Specifically,
we show that harvest focused on the greater-affected sex (males) can result in
stable population dynamics and control of CWD within the next 50 years, given
the constraints of the model. We also provide a quantitative estimate of
geographic disease spread in southern Wisconsin, validating qualitative
assessments that CWD spreads relatively slowly. Given increased discovery and
distribution of CWD throughout North America, insights from our study are
valuable to management agencies and to the general public concerned about the
impacts of CWD on white-tailed deer populations.
snip...
Discussion
CWD Transmission
Using white-tailed deer harvest data from south-central Wisconsin, we show
that FD CWD transmission is the best supported model for both sexes (with higher
infection rates for males) at a broad spatial scale, whereas our earlier efforts
to model this system could not discriminate between FD and DD transmission [18].
It has been suspected that FD was a dominant transmission mechanism in mule deer
[5], [17]; [ but see 6], and more recently in white-tailed deer [28], [46].
Furthermore, our modeling results suggest a more recent and biologically
plausible time since CWD introduction in south-central Wisconsin compared with
earlier analysis [18]. As demonstrated in previous work in this CWD system [21],
[22], [25] and in Colorado [7], [47], adult males have higher CWD infection
rates than females. Although the mechanism for higher CWD infection and
prevalence in males is unknown, these differences may be driven by sex-specific
social behavior [7], [21]. Males typically have larger home ranges, longer
dispersal distances, interactions with other males, or rut-related behavior [48]
that could result in more contacts with infectious deer. In contrast, females
generally interact within a much smaller matrilineal group [27], [28], [49], and
only briefly with males during rut [47].
Given the simplicity of our model, our estimated infection coefficients are
likely a function of several different (and largely unknown) mechanisms that may
vary between/among sexes, seasons, and the environment. These infection rates
represent a weighted average of many potential drivers as summarized by Potapov
et al. [39]. Our models do not account explicitly for indirect transmission from
the environment where prions can persist for years [50], [51], although our
infection rates implicitly subsume both direct and indirect routes of infection.
The importance of environmental transmission has been demonstrated in captive
mule deer [52], [53] and theoretical modeling indicates that population impacts
can be driven by the length of time that prions remain infectious in the
environment [54]. In the long term, the potential accumulation of an
environmental reservoir of infectious prions may become an increasingly
important component of CWD transmission; however, the relative contribution of
direct and indirect transmission in wild deer populations remains unknown and
requires further research. Although we expect infectious contact likely varies
by sex and season, harvest data were insufficient to account for intra-annual
complexity in sex-specific transmission. Additional insights for CWD management
given directional sex-specific transmission (i.e., female-to-male,
female-to-female) may require focal research studies that determine differences
in infectious contact between and among sexes [49], [55]–[57] and how these
influence the risk of disease transmission [28]. In particular, understanding
the mechanisms that lead to rates of male infection twice as high as females
could provide crucial insights on management strategies designed to reduce male
CWD prevalence as an alternative to high male harvest.
Assuming CWD originated in the core area and environmental accumulation of
prions contributes significantly to transmission, we would expect higher
infection rate estimates in the core compared with surrounding areas. We are
uncertain why infection rate is apparently greater in males for some areas to
the west and southwest of the core. These surrounding areas have similar habitat
characteristics with the core, and we would not expect deer abundance to vary
significantly prior to CWD discovery. Heterogeneous harvest management conducted
among areas may be one potential explanation. However, this difference also
suggests that unidentified environmental characteristics or management actions
may influence the current and future trends in CWD prevalence. Regardless, these
patterns suggest that our model predictions for the core area may underestimate
the rate of CWD increase in other areas. Future research is needed to understand
the drivers of CWD transmission, how these vary spatially, and their influence
on future patterns of infection. The identification of potential environmental
reservoirs (e.g., common feeding areas, mineral licks) and evaluation of the
significance of indirect transmission in free-ranging deer populations would
also enhance our ability to predict future trends in infection and allow a
better evaluation of alternative control strategies.
In concept QAIC should help account for overdispersion in our data, which
might result from missing covariates in the model and/or a lack of independence
in the data (e.g., [58]). Such lack of independence may be due to spatial and/or
temporal autocorrelation, and while we do not explicitly account for such
effects, we rely on QAIC to generally accommodate a portion of these impacts.
While we detected significant temporal autocorrelation in residuals for
predicted female prevalence, other research in the same study area [44], [46]
found no spatial autocorrelation in model residuals using a 93.6 km2 or 2.6 km2
spatial frame, respectively. We caution that despite use of QAIC, our model
parameter estimates may still be overly precise.
Rate of spread
Several studies indicate that the southwestern core area of WI is the
likely point of origin for CWD in our study area, with an inverse relationship
between distance-to-core and prevalence as would be expected from an introduced
disease spreading across the landscape [20], [22], [44]. To our knowledge, we
present the first empirical estimate of CWD geographic spread, based on
sex-specific FD transmission, which indicated a low average rate (1.13 km
year−1) during initial phases of the epizootic. There is no current evidence to
suggest that CWD spread in our study area was facilitated by humans (via
movements of infectious animals between game farms or preserves); however, the
anecdotal evidence of such events warrants further investigation. Though DD
transmission was not supported by our data, the estimated rate of geographic
spread was similar for this model structure. Our results suggest that in the
south-central Wisconsin endemic area, CWD has slowly moved across the landscape
and is probably not a recent development. Clearly this estimated rate of spread
must be considered unique to the outbreak in south-central Wisconsin.
Rates of CWD spread in other regions are likely influenced by a number of
factors including habitat features [44], [59], mode of disease transmission,
host species (e.g., white-tailed or mule deer), population structure, host
movements [60], dispersal [61], and possibly the environment [54]. For example,
recent analyses [44] indicate that CWD may be spreading faster from the outbreak
in eastern Wisconsin and northern Illinois than from south-central Wisconsin.
Our simple estimate also assumes an average uniform diffusion from the point of
origin and ignores potential disease movement via longer distance dispersal
[60], although recent discovery of CWD in north-west Wisconsin does not appear
to be linked to long-distance dispersal from southern Wisconsin based on genetic
analysis (S. Robinson Pers. Comm.). In addition, our analysis does not account
for habitat heterogeneity and physical barriers (natural or anthropogenic) that
influence landscape scale movement and interaction of deer populations [62],
[63] or CWD distribution [44], [63]. We also note that despite a highly
significant R2 value, our simple regression utilizes only six data points
(including the core, which we assume is the origin of the epizootic), with
uncertainty that is not accounted for in the regression. As such, there is
likely higher variance associated with our estimated rate of spread.
Despite these limitations, our estimate provides a starting place to
conceptualize early CWD spread across the southern Wisconsin landscape. In the
context of CWD, we believe the areas surrounding the core are currently in
relatively early stages of the epizootic with low, but increasing prevalence.
Under FD transmission and barring effective management efforts, CWD prevalence
is predicted to increase over time, and we suspect that the rate of spread may
also increase because more young males will become infected prior to dispersal
[46]. As such, we consider our spread estimate as a lower bound that is likely
to increase as the epizootic progresses.
Harvest strategies
As a consequence of FD transmission, our simulations predict that in the
next decade CWD prevalence can increase to relatively high levels (25% in
females and 50% in males) in the absence of significant management actions to
reduce infection rates. Of the three harvest strategies we evaluated, only
male-focused harvest succeeded in reducing CWD prevalence below current levels.
Prevalence is reduced because this strategy removes animals from the highest
prevalence class (reducing infection rates), while allowing dilution of
population-level CWD prevalence by recruitment of more females [64]. In
contrast, CWD increased under female-focused and herd-control harvest
strategies. By focusing harvest on the portion of the population with highest
prevalence and infection rates, our simulation suggests that harvest management
can effectively reduce prevalence despite FD disease transmission. Although
disease eradication may not be possible, prevalence reduction (especially in
higher risk groups), which reduces force of infection, is the key to mediating
disease impacts on host populations in the long term. Effective disease
management by sex-specific differential harvest has also been explored for
bovine tuberculosis in deer [55].
The density-dependent harvest structure we imposed produced much lower
average realized harvest (RH) rates for the female-focused and herd-control
strategies, compared with male-focused harvest. High female harvest reduces
population size, which requires lower realized harvest rates to maintain stable
population goals (based on societal tolerance for deer). While this
density-dependent harvest structure is artificial, it is intended to represent
hunter effort in response to perceived deer densities. In the absence of such a
mechanism, static harvest rates over the simulated time frame of 50 years
resulted in host and disease extinction, as predicted in theoretical models of
FD disease transmission [14]. In addition, our results show that deer demography
and CWD dynamics are sensitive to changes in harvest. Estimation of unbiased
harvest rates requires accurate information on both the distribution of
harvested animals and the distribution of the underlying population. Although
harvest-based estimates for deer populations have various limitations [9], [65],
the importance of this parameter for monitoring the performance of CWD
management programs suggests future research to improve estimation procedures
should be considered.
The demographic implications of alternative harvest strategies for disease
management are also important as they affect deer densities, recreational
opportunities (e.g., hunting or observation), and potential disease spread.
While male-focused harvest reduces CWD prevalence in the long term, it results
in lower densities of adult males (compared with herd-control), which are
usually of primary interest to deer hunters. For the herd-control harvest
strategy (current deer management goals) nearly 50% of adult males and 25% of
adult females are expected to become infected within another decade. Even worse,
for female-focused harvest not only are deer densities expected to be low, but
more than 50% of surviving adult males and 30% of adult females would be
infected. In general, these harvest strategies are characterized by accelerating
rates of infection in all deer, and higher prevalence, particularly in males.
Considering the constraints of our model the tradeoff between strategies is
clear; CWD can eventually be reduced with fewer opportunities to harvest healthy
adult bucks, or more adult bucks may be available for harvest, but with higher
rates of CWD infection. Given that quality deer management practices focus on
production of older bucks with large antlers, management agencies could face
difficult alternatives from these competing interests. However, if an
efficacious CWD vaccine was available and cost-effectively distributed to broad
segments of a deer population (particularly males), managers would have more
flexibility to employ a disease control strategy combining harvest and
vaccination to provide adequate recreational opportunities to harvest CWD-free
deer.
The mechanism for density-dependent population regulation in deer is not
well known, but one hypothesis is that deer reduce body size and maintain
survival rates while lowering reproduction [66]. Therefore, we used
density-dependent fecundity to regulate population size in our no-harvest
simulations. The goal of these simulations was to illustrate the rapid increase
in CWD prevalence and eventual impact on deer populations in the absence of
harvest or other factors that remove infected animals prior to mortality from
CWD. Such situations might be likely in high density urban deer populations,
national parks, captive deer farms, or other areas where deer harvest or removal
is limited. This simulation is not designed to represent current conditions in
Wisconsin, and we consider this a worst-case disease scenario in areas without
harvest.
*** However, we also note that CWD transmission rates and prevalence are
much higher in captive deer farms than has been reported in wild populations
[67].
snip...
Conclusions
Given our model structure and data, our results provide strong support for
FD transmission of CWD with the force of infection driven by changes in
prevalence, which we suggest is a vital metric for focused control efforts.
Generally as prevalence increases, as found in Wisconsin, infection rate also
increases in the absence of intervention, producing an accelerating pattern of
infection. Assuming that frequency-dependent transmission predominates (as our
evaluation indicates), management to reduce prevalence will mediate potential
CWD population impacts. The higher rate of infection and prevalence in males,
thus, provides the basis for effective CWD management using deer harvest focused
on this sex. Management to reduce prevalence might be accomplished through the
synergistic effects of targeted harvest and vaccination of males. Unfortunately,
we know little about the mechanisms for male infection and further research is
needed before alternative management strategies to reduce male infection rates
can be developed. Spatial differences in CWD infection rates, despite similar
habitat and pre-CWD deer abundance, suggest that unidentified environmental or
management factors may also influence disease dynamics and future trends in
prevalence. Future research to understand the drivers of CWD transmission, how
these vary spatially, and the relative importance of environmental and direct
transmission is critical to understanding future CWD dynamics in wild
deer.
Our results also indicate that even with high deer densities CWD has been
spreading at a relatively slow rate across the landscape; in agreement with
larger scale spatial patterns for prevalence [44]. However, as disease
prevalence continues to increase, the rate of infection in yearling bucks will
also increase [46]. Because dispersing bucks may be an important source of
disease spread, these patterns suggest that CWD prevalence outside the core area
will continue to grow and the disease may spread at an increasing rate. Although
the drivers of CWD spatial spread are not generally known (see [44] for
identification of landscape features that affect spread), management efforts to
reduce both local prevalence and deer abundance will likely reduce dispersal of
infected yearling bucks. However, the relative impact of reducing deer abundance
versus prevalence in lowering the number of infected yearling bucks likely
depends on disease prevalence and deer density [46]. Further research is needed
to determine the factors that affect spatial spread and develop effective
management strategies.
Figures
Citation: Jennelle CS, Henaux
V, Wasserberg G, Thiagarajan B, Rolley RE, et al. (2014) Transmission of Chronic
Wasting Disease in Wisconsin White-Tailed Deer: Implications for Disease Spread
and Management. PLoS ONE 9(3): e91043.
doi:10.1371/journal.pone.0091043
Editor: Roy Martin Roop II, East Carolina University School of Medicine, United States of America
Received: July 27, 2012; Accepted: February 7, 2014; Published: March 21, 2014
Copyright: © 2014 Jennelle et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: Funding was provided by the Wisconsin Department of Natural Resources and U.S. Geological Survey. The University of Wisconsin Department of Forest and Wildlife Ecology provided assistance with publication costs. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0091043#close
ONCE AGAIN, MANY THANKS TO PLOS ET AL FOR FULL TEXT TO LAYPERSON WITH NO PHD...TSS
Editor: Roy Martin Roop II, East Carolina University School of Medicine, United States of America
Received: July 27, 2012; Accepted: February 7, 2014; Published: March 21, 2014
Copyright: © 2014 Jennelle et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: Funding was provided by the Wisconsin Department of Natural Resources and U.S. Geological Survey. The University of Wisconsin Department of Forest and Wildlife Ecology provided assistance with publication costs. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0091043#close
ONCE AGAIN, MANY THANKS TO PLOS ET AL FOR FULL TEXT TO LAYPERSON WITH NO PHD...TSS
*** However, we also note that CWD transmission rates and prevalence are
much higher in captive deer farms than has been reported in wild populations
[67].
Saturday, March 15, 2014
Potential role of soil properties in the spread of CWD in western Canada
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced
into Great Britain? A Qualitative Risk Assessment October 2012
snip...
In the USA, under the Food and Drug Administration’s BSE Feed Regulation
(21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin)
from deer and elk is prohibited for use in feed for ruminant animals. With
regards to feed for non-ruminant animals, under FDA law, CWD positive deer may
not be used for any animal feed or feed ingredients. For elk and deer considered
at high risk for CWD, the FDA recommends that these animals do not enter the
animal feed system. However, this recommendation is guidance and not a
requirement by law.
Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD
eradication zones and
2) deer and elk that at some time during the 60-month period prior to
slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive
animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from
the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin
processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible
risk___ that (nonruminant) animal feed and pet food containing deer and/or elk
protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data
on the amount of deer and/or elk protein possibly being imported in these
products.
snip...
36% in 2007 (Almberg et al., 2011). In such areas, population declines of
deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of
Colorado, the prevalence can be as high as 30% (EFSA, 2011).
The clinical signs of CWD in affected adults are weight loss and
behavioural changes that can span weeks or months (Williams, 2005). In addition,
signs might include excessive salivation, behavioural alterations including a
fixed stare and changes in interaction with other animals in the herd, and an
altered stance (Williams, 2005). These signs are indistinguishable from cervids
experimentally infected with bovine spongiform encephalopathy (BSE).
Given this, if CWD was to be introduced into countries with BSE such as GB,
for example, infected deer populations would need to be tested to differentiate
if they were infected with CWD or BSE to minimise the risk of BSE entering the
human food-chain via affected venison.
snip...
The rate of transmission of CWD has been reported to be as high as 30% and
can approach 100% among captive animals in endemic areas (Safar et al., 2008).
snip...
In summary, in endemic areas, there is a medium probability that the soil
and surrounding environment is contaminated with CWD prions and in a
bioavailable form. In rural areas where CWD has not been reported and deer are
present, there is a greater than negligible risk the soil is contaminated with
CWD prion.
snip...
In summary, given the volume of tourists, hunters and servicemen moving
between GB and North America, the probability of at least one person travelling
to/from a CWD affected area and, in doing so, contaminating their clothing,
footwear and/or equipment prior to arriving in GB is greater than negligible.
For deer hunters, specifically, the risk is likely to be greater given the
increased contact with deer and their environment. However, there is significant
uncertainty associated with these estimates.
snip...
Therefore, it is considered that farmed and park deer may have a higher
probability of exposure to CWD transferred to the environment than wild deer
given the restricted habitat range and higher frequency of contact with tourists
and returning GB residents.
snip...
*** Spraker suggested an interesting explanation for the occurrence of CWD.
The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr.
Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at
this site. When deer were introduced to the pens they occupied ground that had
previously been occupied by sheep. ...
also, see where even decades back, the USDA had the same thought as they do
today with CWD, not their problem...see page 27 below as well, where USDA stated
back then, the same thing they stated in the state of Pennsylvania, not their
damn business, once they escape, and they said the same thing about CWD in
general back then ;
”The occurrence of CWD must be viewed against the contest of the locations
in which it occurred. It was an incidental and unwelcome complication of the
respective wildlife research programmes. Despite it’s subsequent recognition as
a new disease of cervids, therefore justifying direct investigation, no specific
research funding was forthcoming. The USDA veiwed it as a wildlife problem and
consequently not their province!” ...page 26.
”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.
sound familiar $$$
Sunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
Wednesday, September 04, 2013
*** cwd - cervid captive livestock escapes, loose and on the run in the
wild
how many states have $465,000., and can quarantine and purchase there from,
each cwd said infected farm, but how many states can afford this for all the cwd
infected cervid game ranch type farms ???
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm
Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American
captive herd.
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for
$465,000 for the Statewide Wildlife Habitat Program in Portage County and
approve the restrictions on public use of the site.
SUMMARY:
SEE MORE USAHA REPORTS HERE, 2012 NOT PUBLISHED YET...TSS
Tuesday, February 11, 2014
Wisconsin tracks 81 deer from game farm with CWD buck to seven other states
Friday, March 07, 2014
37th Annual Southeast Deer Study Group Meeting in Athens, Georgia (CWD TSE
Prion abstracts)
Tuesday, February 25, 2014
*** Test results provide current snapshot of CWD in south-central Wisconsin
Dane and Eastern Iowa counties Prevalence has increased in all categories
Monday, March 10, 2014
Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards
Singeltary Submission
$$$
Monday, March 03, 2014
APHIS to Offer Indemnity for CWD Positive Herds as Part of Its Cervid
Health Activities ???
Sunday, March 02, 2014
BIG WIN FOR SHOOTING PENS FROM BRAKKE BLUNDER THANKS TO JUDGE, BIG LOSS FOR
WILD CERVIDS AND POSSIBLE HUMANS FROM CWD
Wednesday, March 05, 2014
Iowa Brakke Family Wins DNR Legal Case
Wednesday, August 21, 2013
IOWA DNR EMERGENCY CONSENT ORDER IN THE MATTER OF TOM & LINDA BRAKKE
D/B/A PINE RIDGE HUNTING LODGE UPDATE AUGUST 21, 2013
snip...
5. On July 16, 2012, DNR received a notice from the Texas Veterinary
Medical Diagnostic Lab ("Texas Vet Lab”) that a sample from an adult male deer
killed at Pine Ridge tested presumptively positive for CWD. (DNR has an
agreement with the Texas Vet Lab to run these preliminary tests.) Because the
Texas Vet Lab found this presumptive positive result, protocols required the
sample to be sent to the National Veterinary Services Laboratory ("National
Lab”) in Ames, Iowa for final confirmation. On July 18, 2012, the National Lab
confirmed the positive CWD result in the deer.
6. On July 19, 2012, DNR notified the Brakkes of the positive test by
phone. Mr. Brakke was out of state.
snip...
12. The Brakkes depopulated the Hunting Preserve, as specified in the
Agreement, from September 10, 2012 to January 31, 2013. As part of this effort,
the Brakkes, the staff and their customers killed 199 captive deer and nine
captive elk. The DNR obtained 170 CWD samples. (Samples were not taken from
fawns and one adult female who was killed in a manner that made sampling
impossible.) Of these 199 deer, two additional adult male deer tested positive
for CWD. Information provided by the Brakkes confirmed that these two additional
deer originated from the Brakke Breeding Facility.
13. DNR installed, with the Brakke's permission, an interior electric fence
on October 1 and 2, 2012.
14. The Brakkes cleaned and disinfected, under DNR supervision, the feeders
and ground surrounding the feeders on April 5, 2013.
15. On April 26, 2013, the Brakkes hand-delivered a notice to the DNR’s
Chief of Law Enforcement Bureau, notifying the DNR that they would no longer
operate a hunting preserve on the Quarantined Premises. The Brakkes did not
reveal any plans to remove the fence around the Quarantined Premises or to
remove the gates to and from the Quarantined Premises in this April 26, 2013
letter.
16. On June 3, 2013, DNR became aware that sections of the exterior fence
surrounding the Quarantined Premises had been removed and that some, if not all,
of the exterior gates to and from the Quarantined Premises were open.
17. On June 4, 2013, DNR received reports from the public in the area that
four wild deer were observed inside the Quarantined Premises.
18. 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.
IV. CONCLUSIONS OF LAW
snip...
Wednesday, August 21, 2013
IOWA DNR EMERGENCY CONSENT ORDER IN THE MATTER OF TOM & LINDA BRAKKE
D/B/A PINE RIDGE HUNTING LODGE UPDATE AUGUST 21, 2013
Thursday, October 03, 2013
TAHC ADOPTS CWD RULE THAT the amendments REMOVE the requirement for a
specific fence height for captives
Texas Animal Health Commission (TAHC) ANNOUNCEMENT October 3, 2013
Tuesday, February 04, 2014
Indiana Hunting preserves Sen. Carlin Yoder Senate Bill 404 and Rep.
William Friend House Bill 1154 DEAD IN THE WATER ?
Saturday, June 29, 2013
PENNSYLVANIA CAPTIVE CWD INDEX HERD MATE YELLOW *47 STILL RUNNING LOOSE IN
INDIANA, YELLOW NUMBER 2 STILL MISSING, AND OTHERS ON THE RUN STILL IN LOUISIANA
Monday, June 24, 2013
The Effects of Chronic Wasting Disease on the Pennsylvania Cervid Industry
Following its Discovery
Tuesday, June 11, 2013
CWD GONE WILD, More cervid escapees from more shooting pens on the loose in
Pennsylvania
Tuesday, May 28, 2013
Chronic Wasting Disease CWD quarantine Louisiana via CWD index herd
Pennsylvania Update May 28, 2013
6 doe from Pennsylvania CWD index herd still on the loose in Louisiana,
quarantine began on October 18, 2012, still ongoing, Lake Charles premises.
Sunday, March 09, 2014
Lesion Profiling and Subcellular Prion Localization of Cervid Chronic
Wasting Disease in Domestic Cats
Monday, December 02, 2013
WISCONSIN CHRONIC WASTING DISEASE CWD DISCOVERED MARATHON COUNTY HUNTING
PRESERVE
Tuesday, December 17, 2013
Wisconsin Second CWD positive deer found in Grant County Second CWD
positive deer found in Grant County
News Release Published: December 16, 2013 by the South Central Region
Contact(s): Tami Ryan, DNR wildlife health, 608-266-3143 Don Bates, CWD
operations. 608- 935-1947 Bob Manwell DNR communications, 608-275-3317
MADISON, Wis. -- A second deer in Grant County from outside the current
chronic wasting disease management zone has tested positive for the disease. The
1.5-year-old buck was killed and registered Nov. 24.
The most recent CWD-positive deer was harvested near the center of the
county about 7.5 miles from the border of the CWD management zone and about four
miles from the first positive which was buck shot during the 2012 season.
“This is why we have focused surveillance around the fringes of the CWD
management zone, to better understand the distribution of the disease and
identify the presence of the disease in periphery areas,” said Don Bates, DNR
CWD operations supervisor. “Based on the 2012 positive deer, and what is known
about the disease and how it spreads, finding another CWD-positive outside the
current zone boundary was not unexpected.”
This is the third year that DNR has focused surveillance around the
boundaries of the existing CWD management zone. Sampling of deer is voluntary in
these areas and in Grant County, DNR partners with private businesses to collect
samples.
“We thank all hunters who brought in deer for voluntary CWD testing during
the nine-day gun season and the businesses that helped us collect samples,”
Bates said. “This cooperation is essential to achieving our goal of detecting
trends in prevalence and distribution of the disease.”
This second positive does not change any remaining hunting seasons nor does
it change the current CWD management zone boundary. Baiting and feeding of deer
is already banned in the county and will continue to be illegal.
For more information on CWD in Wisconsin, and to view CWD management zone
maps, please visit dnr.wi.gov and search keyword “CWD.”
-30-
Tuesday, December 17, 2013
Wisconsin Second CWD positive deer found in Grant County
Monday, December 02, 2013
WISCONSIN CHRONIC WASTING DISEASE CWD DISCOVERED MARATHON COUNTY HUNTING
PRESERVE
CWD-positive White-tailed Deer Found on Marathon County Hunting Preserve
Date: December 2, 2013 Contact: Raechelle Cline, 608-224-5005 or Jim Dick,
Communications Director, 608-224-5020
MADISON – For the first time in five years, a white-tailed deer on a
hunting preserve has tested positive for chronic wasting disease (CWD), State
Veterinarian Dr. Paul McGraw announced today. This latest case was found in
Marathon County.
The National Veterinary Services Laboratory (NVSL) in Ames, Iowa, reported
the final test results back to the state. The animal was a 5-year-old male and
was one of about 370 deer in the 351-acre preserve.
The deer was killed on November 4. Samples were taken on November 7 in
accordance with Wisconsin Department of Agriculture, Trade and Consumer
Protection’s (DATCP’s) rules, which require testing of farm-raised deer and elk
when they die, go to slaughter or are killed. The sample originally tested
positive at a regional laboratory and required a confirmatory test at the NVSL.
The DATCP Animal Health Division’s investigation will look at the animal’s
history and trace movements of deer onto and off the property to determine
whether other herds may have been exposed to the CWD test-positive deer.
McGraw quarantined the preserve and the other three registered farms owned
by the same entity immediately, which stops movement of live deer from the
property, except to slaughter or to their hunting preserves. The business will
be allowed to conduct hunts on the quarantined preserves, because properly
handled dead animals leaving the premises do not pose a disease risk.
This is the first new CWD test-positive deer on a Wisconsin farm since
October 2008.
Since CWD was discovered in Wisconsin in February 2002, there were
eighty-two cases from a single Portage county farm that was depopulated in 2006.
The remaining 15 cases were discovered over a six-year period from 2002 to 2008
on eight farms and hunting preserves. One of the infected animals was an elk;
the rest have been white-tailed deer. Since 1998, more than 35,700 farm-raised
deer and elk have been tested for CWD.
###
12.02.13CWDPositiveMarathon.pdf
UPDATE DECEMBER 3, 2013
The 5-year-old buck was killed Nov. 4 at the Wilderness Game Farm Inc., a
hunting ranch in the Eland area, said Raechelle Cline, public information
officer for the state Division of Animal Health.
The buck was one of about 370 deer in the 351-acre preserve, said State
Veterinarian Dr. Paul McGraw.
Chronic wasting disease, or CWD, is considered a major threat to
Wisconsin’s hunting industry because it can spread from animal to animal and has
been known to devastate herds in other states. In Wisconsin, CWD is confirmed to
have killed fewer than 100 deer, almost all of them on game farms.
Monday, December 02, 2013
WISCONSIN CHRONIC WASTING DISEASE CWD DISCOVERED MARATHON COUNTY HUNTING
PRESERVE
Sunday, November 03, 2013
Wisconsin Second CWD deer found in Portage County
Wisconsin : 436 Deer Have Escaped From Farms to Wild
Date: March 18, 2003 Source: Milwaukee Journal Sentinel snip...
Sunday, November 03, 2013
Wisconsin Second CWD deer found in Portage County
Second CWD deer found in Portage County
News Release
Published: November 1, 2013 by the Northwest Region Contact(s): Kris
Johansen, DNR area wildlife supervisor, 715-284-1430; Ed Culhane,
DNR communications, 715-781-1683 WISCONSIN RAPIDS – A deer harvested by a
bow hunter in southeast Portage County has tested positive for chronic wasting
disease, the state Department of Natural Resources reports. This is the second
CWD-positive wild deer found in the county. Wildlife biologists in central
Wisconsin now are asking bow hunters to assist with increased surveillance for
the disease in four separate areas where positives have been confirmed outside
the CWD management zone.
CWD is contagious and fatal for deer, elk and moose. “Last fall CWD was
discovered for the first time in three wild, white-tailed deer in Adams, Juneau
and Portage counties” said DNR area wildlife supervisor Kris Johansen. “Now we
have a second positive in a different area of Portage County. To better define
the geographic extent of CWD in central Wisconsin, we are focusing additional
surveillance around each of these four locations.”
The latest CWD positive deer was harvested Oct. 6 just northwest of Almond
in Portage County.
To view where the surveillance focus areas are located, hunters can go to
the DNR website and enter “CWD registration” in the key word search, then click
on “CWD registration and sampling.” On this page – http://dnr.wi.gov/topic/wildlifehabitat/registersample.html
– detailed maps show the precise location of these surveillance circles for the
first three positives, the ones in Adams and Juneau counties and the first find
in Portage County, located in the northwest corner of the county.
There is also a map showing the two Portage County locations. A new map,
showing the precise surveillance area for the fourth positive, in southeast
Portage County, will be added to the web page as soon as it is prepared. This
page also links to a list of cooperating taxidermists and meat processors where
samples can be collected.
The DNR is asking hunters to work with these cooperators to have head and
lymph node samples from adult deer – harvested within the four focus areas –
removed for testing. To have the sample removed, the hunter can bring the whole
deer to one of the listed cooperators or just remove the head with at least
three inches of neck attached and bring that in for sampling.
“Please call ahead to set up an appointment,” Johansen said. “These are
private business operators who are helping us out, and we want to respect their
time and their schedules.” This list will be updated online as new cooperators
join the surveillance effort:
• Wisconsin River Meats, N5340 County HH, Mauston 608-847-7413
• A&B Butchering, 6971 Hwy 34, Rudolph 715-435-3893
• Strickly Wild Processing, 140 Buffalo St, Wisconsin Rapids 715-421-0587
• Hartnell's Wild Game Processing, 1925 Cypress Ave., Arkdale 608-339-7288
• Trevor Athens Taxidermy, 982 15th Ave., Arkdale 608-547-6117
• Tall Tines Taxidermy, N2621 Cassidy Road, Mauston 608-547-0818
• Todd's Wildlife Taxidermy, N2148 State 58, Mauston 608-847-7693
• Vollmer Taxidermy, 3631 Plover Road, Plover 715-345-1934
• Field and Stream Taxidermy, 217 S. Front St., Coloma 608-547-1565
• DNR Service Center, 473 Griffith Ave., Wisconsin Rapids 715-421-7813
• Mead Wildlife Area, S2148 County S, Milladore 715-457-6771
• Adams Ranger Station, 532 N. Adams St., Adams 608-339-4819
• Almond Market, 111 Main St., Almond 715-366-2002
Hunters may also have deer from any of the four focus areas tested for CWD
by contacting one of these DNR offices:
• Mead Wildlife Area headquarters, S2148 County S, Milladore – 715-457-6771
• WI Rapids Service Center, 473 Griffith Avenue, Wisconsin Rapids –
715-421-7813
• Adams-Friendship Ranger Station, 532 N. Main Street, Adams – 608-339-4819
On the weekends or during warm periods, hunters should remove the deer head
with at least three inches of neck attached, freeze the head and then contact
the DNR to arrange a drop off. DNR staff will also collect samples from
hunter-harvested deer on the opening weekend of the gun deer season. Collection
stations and hours will be published prior to the gun deer season. The CWD tests
are free to hunters. Each person who submits a head for testing will receive lab
results within three or four weeks. http://dnr.wi.gov/news/BreakingNews_Lookup.asp?id=2996
14 YEARS AGO
THE YEAR 2000
Stop the madness: CWD threatens Wisconsin's elk, deer and, ultimately,
people.
15 July 00
The Isthmus magazine By BRIAN McCOMBIE
Imagine a disease worse than AIDS rippling through Wisconsin's deer herd.
One that's always fatal, cannot be tested for in live animals, and has the
chance of spreading to anyone who eats the infected venison. Sound like the
premise for Michael Crichton's next apocalyptic thriller?
Unfortunately, such a disease already exists in epidemic levels in the
wilds of Colorado and Wyoming. It's infected some game farms, too, and Wisconsin
game farmers have imported more than 350 elk with the potential for this
disease, including elk from farms known to be infected.
"If most people knew what kind of risk this disease poses to free-ranging
deer in the state, they'd be very concerned," says Dr. Sarah Hurley, Lands
Division administrator for the Department of Natural Resources. The DNR is now
testing free-ranging deer around these game farms for the disease: "We're
focusing our energies on those areas where we think there's the greatest
possibility of transmission."
The malady the DNR's looking for is chronic wasting disease (CWD)--better
known, to the extent it is known at all, as mad elk disease. It's a form of the
mad cow disease that devastated Britain's cattle industry in the 1980s, scared
the bejesus out of the populace, and is believed to have killed at least 70
people to date. An elk or deer with CWD can be listless, may walk in circles,
will lose weight and interact progressively less with fellow animals.
The corresponding human affliction is called Creutzfeldt-Jakob disease
(pronounced Croytz-feld Yawkob) or CJD. People with CJD experience symptoms
similar to Alzheimer's, including memory loss and depression, followed by
rapidly progressive dementia and death, usually within one year. While CJD is
rare (literally one in a million odds of getting it), over the last few years at
least three deer hunters have died of it. There is no proof either way whether
they contracted the disease from CWD-infected venison, but new research says it
is possible.
All three varieties--mad cow, mad elk and CJD--belong to a family of
diseases called transmissible spongiform encephalopathy. These diseases alter
the conformation of proteins in the brain called prions; after-death brain
samples usually show a series of microscopic holes in and around brain cells.
No one is exactly sure how mad elk disease spreads. At first, transmittal
through blood seemed likely, as from mother to fawn. But CWD has moved between
adult animals at game farms, leading scientists to conclude that it can be
spread through saliva or simple contact. Also, the rates of transmission are
higher in areas where animals have the most opportunities for contact.
Wisconsin's concentrated population of 1.7 million deer interact freely with
each other, and scientific modeling suggests CWD could tear through our deer
herd devastatingly fast. Despite the danger, Wisconsin and other states are
relying on only sporadic testing and a system of voluntary compliance. It's a
system that some say has more holes in it than a CWD-infected brain.
At present, Wisconsin game farm owners, even those harboring elk and deer
brought in from farms with known cases of CWD, do not have to call a
veterinarian if a deer or elk suddenly dies or acts strange. They're also not
required to inform the state Department of Natural Resources (DNR) or the
Department of Agriculture, Trade and Consumer Protection (DATCP) if animals
escape into the wild.
"The lax attitude is pretty shocking," says John Stauber, a Madison
activist and co-author of Mad Cow U.S.A. To protect people and deer, Stauber
argues for an immediate importation ban for game farms, plus programs of testing
and surveillance. He suggests both DATCP and DNR aren't taking such measures
because, as the regulators in charge, they don't want to find the CWD he thinks
is likely already in state. "It's in their bureaucratic interest to not
[actively] look for CWD in the game farms," says Stauber. "Because if they find
it, who's to blame?"
In the wild and especially out west, chronic wasting disease is spreading
fast. Northeastern Colorado documented its first case in 1981. By the mid-1990s,
samplings of mule deer brains showed 3% to 4% testing positive for CWD. Within a
few years, the rate was 8%, and now Larimer County, the center of the endemic
area, has a 15% rate of infection among mule deer. It's also being found in deer
and elk in Wyoming.
"Fifteen percent of a wild population of animals with this disease is
staggering," says Dr. Thomas Pringle, who tracks CWD-type diseases for the
Sperling Biomedical Foundation in Eugene, Ore. "It's basically unheard of. This
appears to be an unusually virulent strain. with highly efficient horizontal
transmission mechanisms."
CWD could eventually spread to Wisconsin on its own, animal to animal. But
that would take decades. Game farms, though, provide a mechanism to cut through
all that time and distance and drop CWD smack in the middle of the state.
An open-records search by Isthmus reveals that the first shipment of farm
elk from areas with CWD in the wild occurred in 1992, with 66 Colorado elk going
to a game farm in Plymouth. In April 1998, DATCP was informed that a Bloomer
game farm had purchased one elk from a Nebraska farm later found to be
CWD-infected. This prompted a Sept. 15, 1998, memo from Steven Miller, head of
the DNR's Lands Division, to Secretary George Meyer, with copies to DATCP chief
Ben Brancel and Gov. Tommy Thompson. In it, Miller recommends that Wisconsin
follow the lead of Montana (which found CWD on two game farms) and place "a
moratorium on the importation of all game farm animals.... At present it appears
the only way to help assure the disease does not spread into Wisconsin."
But the moratorium was never put in place, so it's possible that even more
elk potentially carrying CWD are now in state.
Instead of a moratorium, Wisconsin has opted for testing. It is among 12
states and two Canadian provinces that currently test deer for CWD. Last year,
the Wisconsin DNR began testing road- and hunter-killed deer in 1999 within a
five-mile radius of game farms that have brought in elk from CWD-infected areas.
Test areas include all or part of Fond du Lac, Dodge, Jefferson, Sheboygan and
Washington counties. All of the approximately 250 brains examined in 1999 came
back negative; this year, 500 to 600 deer will be tested.
Meanwhile, DATCP is asking owners of game farms that have animals from
herds known to have cases of CWD infection to voluntarily enter a surveillance
program. The agency's top veterinarian, Dr. Clarence Siroky, argues that
voluntary compliance makes more sense than a moratorium because, ban or no ban,
game farm operators "are going to find a way to bring these animals into the
state. We don't have police patrols and impregnable borders to keep anything in
or out."
With voluntary compliance, Siroky says, at least there are records of
animals entering the state. So if CWD or other diseases are discovered, the
animals can be traced back to their original herds and other farms they may have
been at. "It's better to know where the animals are coming in from," he insists.
Siroky may be right that an importation ban would result in some game farms
smuggling in animals. But currently, game farmers can bring in any deer or elk,
even those from known CWD-infected areas, so long as they can produce a health
certificate showing the animal's been tested. The problem is that no test exists
to find CWD in live animals. Animals can carry CWD for years and still look
healthy, so some of the 370 elk shipped into Wisconsin between 1996 and 1999
from CWD areas could have the disease. The odds are even higher for animals
purchased from farms later found to have CWD.
Wisconsin has approximately 100 deer or elk farms and they're big business.
On the Internet, prices for elk calves start at $1,500, and breeding bulls go
for up to $20,000. Some farms sell venison and the velvet that peels from new
elk antlers (considered an aphrodisiac in Asia). Others offer "hunts" costing
between $1,000 and $5,000 for trophy deer, to more than $10,000 for bull elk
with massive antlers.
Given these economics, it's reasonable to question why anyone with a
suspicion of CWD in his or her herd would call in state regulators or a vet. A
farm with a proven CWD case, confirms Dr. Robert Ehlenfeldt, DATCP's director of
Animal Disease Control, would be shut down indefinitely.
And if a problem develops on a Wisconsin game farm, there's no guarantee
that's where it will stay. Dr. Hurley says even fenced-in animals have easy
nose-to-nose contact with wild and other farmed animals. Besides, as the DNR's
chief of special operations Thomas Solin has documented, many game farms are not
secure. Gates are sometimes left open. Fences rust and break, rot and topple,
get crushed by fallen trees. Even if game farm animals don't escape, such
breaches allow wild deer to get in, mingle with the farmed deer and elk, then
leave.
Unlike other diseases, there's no test for CWD in living animals because it
doesn't create an immune system counter-response, detectable through blood
analysis. You can't kill CWD and related diseases by cooking the meat. One test
Stauber recounts in Mad Cow U.S.A. found that scrapie, a sheep form of CWD,
stayed viable after a full hour at 680 degrees Fahrenheit. Most disinfectants
don't kill these diseases, either, and they can exist in the soil for years.
And while diseases like mad cow and mad elk do have some trouble jumping
from species to species, it can happen. This May, Byron Caughey of the National
Institutes of Health announced that he had converted human brain materials with
mad-elk-contaminated brain matter at rates roughly equal to the transfer between
mad cow and humans.
Says Dr. Pringle, referring to Caughey's work, "CWD may not transmit that
easily, but the rate isn't zero." Pringle notes that the test Caughey used has
been a very reliable proxy in the past in determining transmission possibilities
for other diseases, including mad cow.
Once they jump the species barrier, transmissible spongiform encephalopathy
diseases adapt to fit the new host and are then passed on rather easily within
that species. Unfortunately, says Pringle, no one is trying to determine if CWD
has jumped into people as Creutzfeldt-Jakob disease. Making matters more
difficult is the fact that the disease can incubate for decades before symptoms
are seen.
In states with CWD-infected deer, thousands of people have undoubtedly been
exposed to CWD-infected venison. A February 1998 Denver Post article tells of
one hunter who's venison tested positive for CWD. By the time he was notified,
his meat had already been ground up and mixed with meat from hundreds of other
deer for venison sausage.
With AIDS, Pringle notes, there was a definite overreaction, with people
initially afraid to even shake hands with people infected with the virus.
Looking at the CWD situation in Colorado, he says there's been complete
underreaction. "It's like, oh, what the hell. Nobody's died yet--so keep eating
the venison!'" Pringle worries that if the disease is found in humans, it will
be so only after years of spreading through the human community.
Looking over documents obtained by Isthmus through its open-records
request, Stauber says DATCP is behaving more like a lobbyist for the game farm
industry than an agency bent on protecting Wisconsin's people from CWD. He
points to DATCP's Cervidae Advisory Committee as a prime example. In a Nov. 11,
1998, memo from Siroky to DATCP secretary Ben Brancel, Siroky notes that the
committee is needed to "obtain information from the public concerning disease
regulation" of farmed deer and elk, and "to help formulate action plans for
importation requirements, prevention and control" of CWD. But of the 12 people
Siroky nominates, one's a DNR warden, one's a DATCP employee, and the other 10
are game farm owners. And two of these owners were among those DATCP knew had
purchased elk from farms at high risk of having CWD.
"There's no significant input from anyone else," says Stauber. "Farmers,
deer hunters and consumers are all left out. Meanwhile, the government's failing
to take all necessary precautions to alert the public to this potential health
threat."
Friday, February 03, 2012
Wisconsin Farm-Raised Deer Farms and CWD there from 2012 report Singeltary
et al
*** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***
Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014
*** 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.
*** The potential impact of prion diseases on human health was greatly
magnified by the recognition that interspecies transfer of BSE to humans by beef
ingestion resulted in vCJD. While changes in animal feed constituents and
slaughter practices appear to have curtailed vCJD, there is concern that CWD of
free-ranging deer and elk in the U.S. might also cross the species barrier.
Thus, consuming venison could be a source of human prion disease. Whether BSE
and CWD represent interspecies scrapie transfer or are newly arisen prion
diseases is unknown. Therefore, the possibility of transmission of prion disease
through other food animals cannot be ruled out. There is evidence that vCJD can
be transmitted through blood transfusion. There is likely a pool of unknown size
of asymptomatic individuals infected with vCJD, and there may be asymptomatic
individuals infected with the CWD equivalent. These circumstances represent a
potential threat to blood, blood products, and plasma supplies.
The chances of a person or domestic animal contracting CWD are “extremely
remote,” Richards said. The possibility can’t be ruled out, however. “One could
look at it like a game of chance,” he explained. “The odds (of infection)
increase over time because of repeated exposure. That’s one of the downsides of
having CWD in free-ranging herds: We’ve got this infectious agent out there that
we can never say never to in terms of (infecting) people and domestic
livestock.”
Thursday, March 20, 2014
*** CHRONIC WASTING DISEASE CWD TSE PRION OF CERVID AND THE POTENTIAL FOR
HUMAN TRANSMISSION THEREFROM 2014 ***
Friday, November 09, 2012
*** Chronic Wasting Disease CWD in cervidae and transmission to other
species
Sunday, November 11, 2012
*** Susceptibilities of Nonhuman Primates to Chronic Wasting Disease
November 2012
Friday, December 14, 2012
Susceptibility Chronic Wasting Disease (CWD) in wild cervids to Humans 2005
- December 14, 2012
Saturday, March 09, 2013
Chronic Wasting Disease in Bank Voles: Characterisation of the Shortest
Incubation Time Model for Prion Diseases
Thursday, January 2, 2014
*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant
Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***
WHAT about the sporadic CJD TSE proteins ?
WE now know that some cases of sporadic CJD are linked to atypical BSE and
atypical Scrapie, so why are not MORE concerned about the sporadic CJD, and all
it’s sub-types $$$
Creutzfeldt-Jakob Disease CJD cases rising North America updated report
August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada
seeing an extreme increase of 48% between 2008 and 2010 ***
Sunday, October 13, 2013
*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
Sunday, March 09, 2014
A Creutzfeldt-Jakob Disease (CJD) Lookback Study: Assessing the Risk of
Blood Borne Transmission of Classic Forms of Creutzfeldt-Jakob Disease
FDA TSEAC CIRCUS AND TRAVELING ROAD SHOW FOR THE TSE PRION DISEASES
Wednesday, December 11, 2013
*** Detection of Infectivity in Blood of Persons with Variant and Sporadic
Creutzfeldt-Jakob Disease ***
Monday, February 10, 2014
18 Forsyth Medical Center patients exposed to CJD; apology issued...OOOPS,
SORRY, TOO BAD $$$
Tuesday, February 11, 2014
Novant Health Forsyth Medical Center Information on potential CJD exposure
Monday, February 3, 2014
*** Evaluation of the zoonotic potential of transmissible mink
encephalopathy TSE Prion disease
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF
TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Sunday, March 23, 2014
APHIS USDA National Scrapie Eradication Program February 2014 Monthly
Report Fiscal Year 2014
Monday, March 3, 2014
*** Gov. C.L. "Butch" Otter of Idaho signs bill that will force consumers
to eat dead stock downers and whatever else the industry decides
see updated Rancho CLASS 1 HIGH RISK dead stock cancer downer recall for
IDAHO
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
OAI 2012-2013
OAI (Official Action Indicated) when inspectors find significant
objectionable conditions or practices and believe that regulatory sanctions are
warranted to address the establishment’s lack of compliance with the regulation.
An example of an OAI classification would be findings of manufacturing
procedures insufficient to ensure that ruminant feed is not contaminated with
prohibited material. Inspectors will promptly re-inspect facilities classified
OAI after regulatory sanctions have been applied to determine whether the
corrective actions are adequate to address the objectionable conditions.
ATL-DO 1035703 Newberry Feed & Farm Ctr, Inc. 2431 Vincent St. Newberry
SC 29108-0714 OPR DR, FL, FR, TH HP 9/9/2013 OAI Y
DET-DO 1824979 Hubbard Feeds, Inc. 135 Main, P.O. Box 156 Shipshewana IN
46565-0156 OPR DR, FL, OF DP 8/29/2013 OAI Y
ATL-DO 3001460882 Talley Farms Feed Mill Inc 6309 Talley Rd Stanfield NC
28163-7617 OPR FL, TH NP 7/17/2013 OAI N
NYK-DO 3010260624 Sherry Sammons 612 Stoner Trail Rd Fonda NY 12068-5007
OPR FR, OF NP 7/16/2013 OAI Y
DEN-DO 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO
81067 OPR RE, TH HP 2/27/2013 OAI N
CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR
FR, OF HP 11/26/2012 OAI Y
*** DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO
80631-9501 OPR RE, TH HP 10/12/2012 OAI N
Ruminant Feed Inspections Firms Inventory (excel format)
PLEASE NOTE, the VAI violations were so numerous, and unorganized in dates
posted, as in numerical order, you will have to sift through them for
yourselves. ...tss
snip...see full text ;
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
Saturday, December 15, 2012
Bovine spongiform encephalopathy: the effect of oral exposure dose on
attack rate and incubation period in cattle -- an update 5 December 2012
Sunday, February 2, 2014
The Presence of Disease-Associated Prion Protein in Skeletal Muscle of
Cattle Infected with Classical Bovine Spongiform Encephalopathy
NOTE Pathology
Saturday, December 21, 2013
**** Complementary studies detecting classical bovine spongiform
encephalopathy infectivity in jejunum, ileum and ileocaecal junction in
incubating cattle ****
Wednesday, December 4, 2013
*** Bovine Spongiform Encephalopathy; Importation of Bovines and Bovine
Products; Final Rule Federal Register / Vol. 78 , No. 233 /
Wednesday, December 4, 2013
Saturday, November 2, 2013
*** APHIS Finalizes Bovine Import Regulations in Line with International
Animal Health Standards while enhancing the spread of BSE TSE prion mad cow type
disease around the Globe
*** 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.
Friday, March 21, 2014
Rancho Dead Stock Cancer Downers Recall Explained FSIS March 20 2014
?
“As of March 20, 2014, FSIS has completed all checks (effectiveness checks
and disposition verification checks) for recalls 002-2014 and 013-2014 regarding
Rancho Feeding Corporation. FSIS has determined that based on the number of
successful checks (see Directive 8080.1, Attachment 1, Table 3) where businesses
were notified of the recall and removed affected products from commerce that the
recall activities were effective.”
say what $$$
Monday, December 1, 2008
When Atypical Scrapie cross species barriers
why do we not want to do TSE transmission studies on chimpanzees $
snip...
5. A positive result from a chimpanzee challenged severly would likely
create alarm in some circles even if the result could not be interpreted for
man. I have a view that all these agents could be transmitted provided a large
enough dose by appropriate routes was given and the animals kept long enough.
Until the mechanisms of the species barrier are more clearly understood it might
be best to retain that hypothesis.
snip...
R. BRADLEY
1: J Infect Dis 1980 Aug;142(2):205-8
Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.
Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.
Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep
and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were
exposed to the infectious agents only by their nonforced consumption of known
infectious tissues. The asymptomatic incubation period in the one monkey exposed
to the virus of kuru was 36 months; that in the two monkeys exposed to the virus
of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the
two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively.
Careful physical examination of the buccal cavities of all of the monkeys failed
to reveal signs or oral lesions. One additional monkey similarly exposed to kuru
has remained asymptomatic during the 39 months that it has been under
observation.
snip...
The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie
by natural feeding to squirrel monkeys that we have reported provides further
grounds for concern that scrapie-infected meat may occasionally give rise in
humans to Creutzfeldt-Jakob disease.
PMID: 6997404
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract
Recently the question has again been brought up as to whether scrapie is
transmissible to man. This has followed reports that the disease has been
transmitted to primates. One particularly lurid speculation (Gajdusek 1977)
conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and
transmissible encephalopathy of mink are varieties of a single "virus". The U.S.
Department of Agriculture concluded that it could "no longer justify or permit
scrapie-blood line and scrapie-exposed sheep and goats to be processed for human
or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is
emphasised by the finding that some strains of scrapie produce lesions identical
to the once which characterise the human dementias"
Whether true or not. the hypothesis that these agents might be
transmissible to man raises two considerations. First, the safety of laboratory
personnel requires prompt attention. Second, action such as the "scorched meat"
policy of USDA makes the solution of the acrapie problem urgent if the sheep
industry is not to suffer grievously.
snip...
76/10.12/4.6
Nature. 1972 Mar 10;236(5341):73-4.
Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).
Gibbs CJ Jr, Gajdusek DC.
Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0
Transmission of Scrapie to the Cynomolgus Monkey (Macaca
fascicularis)
C. J. GIBBS jun. & D. C. GAJDUSEK
National Institute of Neurological Diseases and Stroke, National Institutes
of Health, Bethesda, Maryland
SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey
(Macaca fascicularis) with an incubation period of more than 5 yr from the time
of intracerebral inoculation of scrapie-infected mouse brain. The animal
developed a chronic central nervous system degeneration, with ataxia, tremor and
myoclonus with associated severe scrapie-like pathology of intensive astroglial
hypertrophy and proliferation, neuronal vacuolation and status spongiosus of
grey matter. The strain of scrapie virus used was the eighth passage in Swiss
mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral
passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton,
Berkshire).
Re: vCJD in the USA * BSE in U.S. 15 November 1999 Terry S Singeltary, NA
CWD is just a small piece of a very big puzzle. I have seen while deer
hunting, deer, squirrels and birds, eating from cattle feed troughs where they
feed cattle, the high protein cattle by products, at least up until Aug. 4,
1997. So why would it be so hard to believe that this is how they might become
infected with a TSE. Or, even by potentially infected land. It's been well
documented that it could be possible, from scrapie.
It was proven in Oprah Winfrey's trial, that Cactus Cattle feeders, sent
neurologically ill cattle, some with encephalopathy stamped on the dead slips,
were picked up and sent to the renders, along with sheep carcasses.
U.S. Scientist should be concerned with a CJD epidemic in the U.S., as
well...
2 January 2000 Terry S Singeltary
The exact same recipe for B.S.E. existed in the U.S. for years and years.
In reading over the Qualitative Analysis of BSE Risk Factors-1, this is a 25
page report by the USDA:APHIS:VS. It could have been done in one page. The first
page, fourth paragraph says it all;
"Similarities exist in the two countries usage of continuous rendering
technology and the lack of usage of solvents, however, large differences still
remain with other risk factors which greatly reduce the potential risk at the
national level."
Then, the next 24 pages tries to down-play the high risks of B.S.E. in the
U.S., with nothing more than the cattle to sheep ratio count, and the
geographical locations of herds and flocks. That's all the evidence they can
come up with, in the next 24 pages.
Something else I find odd, page 16;
"In the United Kingdom there is much concern for a specific continuous
rendering technology which uses lower temperatures and accounts for 25 percent
of total output. This technology was _originally_ designed and imported from the
United States. However, the specific application in the production process is
_believed_ to be different in the two countries."
A few more factors to consider, page 15;
"Figure 26 compares animal protein production for the two countries. The
calculations are based on slaughter numbers, fallen stock estimates, and product
yield coefficients. This approach is used due to variation of up to 80 percent
from different reported sources. At 3.6 million tons, the United States produces
8 times more animal rendered product than the United Kingdom."
"The risk of introducing the BSE agent through sheep meat and bone meal is
more acute in both relative and absolute terms in the United Kingdom (Figures 27
and 28). Note that sheep meat and bone meal accounts for 14 percent, or 61
thousand tons, in the United Kingdom versus 0.6 percent or 22 thousand tons in
the United States. For sheep greater than 1 year, this is less than one-tenth of
one percent of the United States supply."
"The potential risk of amplification of the BSE agent through cattle meat
and bone meal is much greater in the United States where it accounts for 59
percent of total product or almost 5 times more than the total amount of
rendered product in the United Kingdom."
Considering, it would only take _one_ scrapie infected sheep to contaminate
the feed. Considering Scrapie has run rampant in the U.S. for years, as of Aug.
1999, 950 scrapie infected flocks. Also, Considering only one quarter spoonful
of scrapie infected material is lethal to a cow. Considering all this, the sheep
to cow ration is meaningless. As I said, it's 24 pages of B.S.e.
To be continued...
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA
Competing interests: None declared
Letters
JAMA. 2001;285(6):733-734. doi: 10.1001/jama.285.6.733
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Terry S. Singeltary, Sr Bacliff, Tex
Since this article does not have an abstract, we have provided the first
150 words of the full text.
KEYWORDS: creutzfeldt-jakob disease, diagnosis. 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.
References 1. Gibbons RV, Holman RC, Belay ED, Schonberger LB.
Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA.
2000;284:2322-2323.
Published March 26, 2003
RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease
in the United States
Terry S. Singeltary, retired (medically)
I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment
on the CDC's attempts to monitor the occurrence of emerging forms of CJD.
Asante, Collinge et al [1] have reported that BSE transmission to the
129-methionine genotype can lead to an alternate phenotype that is
indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD
and all human TSEs are not reportable nationally. CJD and all human TSEs must be
made reportable in every state and internationally. I hope that the CDC does not
continue to expect us to still believe that the 85%+ of all CJD cases which are
sporadic are all spontaneous, without route/source. We have many TSEs in the USA
in both animal and man. CWD in deer/elk is spreading rapidly and CWD does
transmit to mink, ferret, cattle, and squirrel monkey by intracerebral
inoculation. With the known incubation periods in other TSEs, oral transmission
studies of CWD may take much longer. Every victim/family of CJD/TSEs should be
asked about route and source of this agent. To prolong this will only spread the
agent and needlessly expose others. In light of the findings of Asante and
Collinge et al, there should be drastic measures to safeguard the medical and
surgical arena from sporadic CJDs and all human TSEs. I only ponder how many
sporadic CJDs in the USA are type 2 PrPSc?
Published March 26, 2003
14th ICID International Scientific Exchange Brochure - Final Abstract
Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North
America update October 2009
T. Singeltary Bacliff, TX, USA
Background: An update on atypical BSE and other TSE in North America.
Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE
have all been documented in North America, along with the typical scrapie's, and
atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME.
All these TSE in different species have been rendered and fed to food producing
animals for humans and animals in North America (TSE in cats and dogs ?), and
that the trading of these TSEs via animals and products via the USA and Canada
has been immense over the years, decades.
Methods: 12 years independent research of available data
Results: I propose that the current diagnostic criteria for human TSEs only
enhances and helps the spreading of human TSE from the continued belief of the
UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to
continue to validate this old myth, will only spread this TSE agent through a
multitude of potential routes and sources i.e. consumption, medical i.e.,
surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics
etc.
Conclusion: I would like to submit a review of past CJD surveillance in the
USA, and the urgent need to make all human TSE in the USA a reportable disease,
in every state, of every age group, and to make this mandatory immediately
without further delay. The ramifications of not doing so will only allow this
agent to spread further in the medical, dental, surgical arena's. Restricting
the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD
knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante,
Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis,
Marsh, et al and many more, that the world of TSE Transmissible Spongiform
Encephalopathy is far from an exact science, but there is enough proven science
to date that this myth should be put to rest once and for all, and that we move
forward with a new classification for human and animal TSE that would properly
identify the infected species, the source species, and then the route.
The Lancet Infectious Diseases, Volume 3, Issue 8, Page 463, August 2003
doi:10.1016/S1473-3099(03)00715-1Cite or Link Using DOI
Tracking spongiform encephalopathies in North America
Original
Xavier Bosch
“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.” 49-year—old Singeltary is
one of a number of people who have remained largely unsatisfied after being told
that a close relative died from a rapidly progressive dementia compatible with
spontaneous Creutzfeldt—Jakob ...
SEE FULL TEXT ;
-------- Original Message --------
Subject: Tracking spongiform encephalopathies in North America LANCET
INFECTIOUS DISEASE Volume 3, Number 8 01 August 2003
Date: Tue, 29 Jul 2003 17:35:30 –0500
From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
Volume 3, Number 8 01 August 2003
Previous
Next
Newsdesk
Tracking spongiform encephalopathies in North America
Xavier Bosch
My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my
mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever
since. What I have found is that we have not been told the truth. CWD in deer
and elk is a small portion of a much bigger problem.
49-year-old Singeltary is one of a number of people who have remained
largely unsatisfied after being told that a close relative died from a rapidly
progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease
(CJD). So he decided to gather hundreds of documents on transmissible spongiform
encephalopathies (TSE) and realised that if Britons could get variant CJD from
bovine spongiform encephalopathy (BSE), Americans might get a similar disorder
from chronic wasting disease (CWD)the relative of mad cow disease seen among
deer and elk in the USA. Although his feverish search did not lead him to the
smoking gun linking CWD to a similar disease in North American people, it did
uncover a largely disappointing situation.
Singeltary was greatly demoralised at the few attempts to monitor the
occurrence of CJD and CWD in the USA. Only a few states have made CJD
reportable. Human and animal TSEs should be reportable nationwide and
internationally, he complained in a letter to the Journal of the American
Medical Association (JAMA 2003; 285: 733). I hope that the CDC does not continue
to expect us to still believe that the 85% plus of all CJD cases which are
sporadic are all spontaneous, without route or source.
Until recently, CWD was thought to be confined to the wild in a small
region in Colorado. But since early 2002, it has been reported in other areas,
including Wisconsin, South Dakota, and the Canadian province of Saskatchewan.
Indeed, the occurrence of CWD in states that were not endemic previously
increased concern about a widespread outbreak and possible transmission to
people and cattle.
To date, experimental studies have proven that the CWD agent can be
transmitted to cattle by intracerebral inoculation and that it can cross the
mucous membranes of the digestive tract to initiate infection in lymphoid tissue
before invasion of the central nervous system. Yet the plausibility of CWD
spreading to people has remained elusive.
Part of the problem seems to stem from the US surveillance system. CJD is
only reported in those areas known to be endemic foci of CWD. Moreover, US
authorities have been criticised for not having performed enough prionic tests
in farm deer and elk.
Although in November last year the US Food and Drug Administration issued a
directive to state public-health and agriculture officials prohibiting material
from CWD-positive animals from being used as an ingredient in feed for any
animal species, epidemiological control and research in the USA has been quite
different from the situation in the UK and Europe regarding BSE.
Getting data on TSEs in the USA from the government is like pulling teeth,
Singeltary argues. You get it when they want you to have it, and only what they
want you to have.
Norman Foster, director of the Cognitive Disorders Clinic at the University
of Michigan (Ann Arbor, MI, USA), says that current surveillance of prion
disease in people in the USA is inadequate to detect whether CWD is occurring in
human beings; adding that, the cases that we know about are reassuring, because
they do not suggest the appearance of a new variant of CJD in the USA or
atypical features in patients that might be exposed to CWD. However, until we
establish a system that identifies and analyses a high proportion of suspected
prion disease cases we will not know for sure. The USA should develop a system
modelled on that established in the UK, he points out.
Ali Samii, a neurologist at Seattle VA Medical Center who recently reported
the cases of three hunterstwo of whom were friendswho died from pathologically
confirmed CJD, says that at present there are insufficient data to claim
transmission of CWD into humans; adding that [only] by asking [the questions of
venison consumption and deer/elk hunting] in every case can we collect suspect
cases and look into the plausibility of transmission further. Samii argues that
by making both doctors and hunters more aware of the possibility of prions
spreading through eating venison, doctors treating hunters with dementia can
consider a possible prion disease, and doctors treating CJD patients will know
to ask whether they ate venison.
CDC spokesman Ermias Belay says that the CDC will not be investigating the
[Samii] cases because there is no evidence that the men ate CWD-infected meat.
He notes that although the likelihood of CWD jumping the species barrier to
infect humans cannot be ruled out 100% and that [we] cannot be 100% sure that
CWD does not exist in humans& the data seeking evidence of CWD transmission
to humans have been very limited.
LANCET SINGELTARY ET AL CWD TSE PRION NORTH AMERICA
http://download.thelancet.com/pdfs/journals/laninf/PIIS1473309903007151.pdf?id=baa1CkXPkhI3Ih_Vlh6ru
Singeltary submission to PLOS ;
No competing interests declared.
see full text ;
Owens, Julie
From: Terry S. Singeltary Sr. [flounder9@verizon.net]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE) Page 1 of 98
FSIS, USDA, REPLY TO SINGELTARY
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary...
2009
Tuesday, August 18, 2009
* BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
Monday, March 10, 2014
Investigators study silent variant of mad cow disease Galveston Daily News
March 4, 2014
Wednesday, May 16, 2012
*** Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion
disease, Iatrogenic, what if ?
Proposal ID: 29403
CJD QUESTIONNAIRE USA
CJD VOICE
never break a promise to your mom. DOD 12/14/97 CONFIRMED hvCJD...
layperson
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net
posted by Terry S. Singeltary Sr. at
1:31 PM
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