Wednesday, April 18, 2007

PENNSYLVANIA NEWS: Game Commission Board of Directors Vs. Biologists

Rooney's two cents: Hey Thomas Boop--of course you would never run a business this way. Then again, (1) this is not a business, which is a good thing, because (2) the price of deer tags does not include many of the economic costs of deer damage, such as auto collisions and medical treatment, crop and landscape damage, disease transmission to humans and livestock, and damage to forests and forestry. I'm all for your proposal to fix the "fatal flaws" in the deer management program if you are all for adding these externalities into the price of tags. I think hunters might balk at the $200-300 price per tag, though (based on some back of the envelope calculations).

HARRISBURG, Pa. - The president of the Pennsylvania Game Commission's board of directors said Tuesday the agency's controversial deer-management plan is "fatally flawed."

"We would never run a business the way we're running our deer-management program," board president Thomas E. Boop said.

Just a few hours after Boop delivered his stinging criticism of the program, the agency biologists responsible for that program recommended continuing it with virtually no changes for the upcoming 2007-08 hunting season.

"We're going to base our information and recommendations on the best science that we can and on the best data that we can," said Cal DuBrock, head of the Game Commission's Bureau of Wildlife Management.

Tuesday was the first day of the Game Commission's annual, two-day spring meeting, at which hunting and trapping seasons and bag limits for the state's game animals are set for the following fall and winter. The commissioners will vote today to set those seasons and bag limits.

As has been the case over the past decade, deer and deer management proved to be the most discussed and most controversial topics of the meeting's first day.

Hunters lined up to tell the commissioners the deer herd across the state has been decimated by years of overhunting.

"To stay the course (with the management program) would adversely affect the sport of hunting for all ages in our state," said East Hempfield Township resident Charles Bolgiano, who is legislative liaison for Unified Sportsmen of Pennsylvania.

Likewise, forest managers and people interested in seeing diversified wildlife and plant life lined up to encourage the commissioners not to alter the course of the deer-management program.

"We are finally seeing signs of recovery in forest regeneration," said Jim Chapman, a forest manager who works for a lumber company in Warren County.

Wildlife biologist Chris Rosenberry, who heads the Game Commission's deer-management division, agreed with Chapman's assessment, and said now is not the time to reverse course on the program.

The health of the state's deer and the health of the state's forest, Rosenberry said, indicate the Game Commission must keep up the current amount of hunting pressure applied to the deer herd.

As a result, Rosenberry recommended the commissioners vote today to maintain last year's slate of hunting seasons, with the exception of extending it in part of the southeast region, where deer numbers are particularly high.

He also recommended the commissioners allocate 6,000 more antlerless deer licenses than they issued last year, for a total of 865,000 licenses.

The Game Commission controls the state's deer population by regulating the number of female deer that are killed each year.

Each license allows a hunter to kill one antlerless deer, which is either a doe, a buck that's too young to have grown antlers or an older buck that has lost its antlers.

State Rep. Sam Rohrer of Berks County, who is the minority chairman of the House Game & Fisheries Committee, said more people from across the state complain to him about the deer-management program than any other issue.

Hunters are complaining to their legislators about the lack of deer, Rohrer said, because the hunters believe the Game Commission isn't listening to their opinions.

Rohrer said the Game Commission's data regarding the state's deer herd sometimes contradicts itself. He recommended the agency submit to an independent audit of its facts and figures.

Boop supported Rohrer's proposal, saying he "can't make any sense out of the data I've seen."

Rohrer said he believes the Legislature would help finance and facilitate the audit if the Game Commission would submit to it.

And he recommended the agency suspend all antlerless deer hunting by adults during the annual two-week firearms deer season this fall until the audit is conducted.

"All I'm asking for is a little bit of a break in the program so that we can focus on the data collection," Rohrer said.



Terry S. Singeltary Sr. said...

Greetings PGC,

I thought I might send you this update on CWD. please circulate as you wish. ...terry


Survival of PrPSc during Simulated Wastewater Treatment Processes

Pedersen, J1; Hinckley, G1; McMahon, K2; McKenzie, D3; Aiken, JM3
1University of Wisconsin, Soil Science/Civil and Environmental Engineering,
USA; 2University of Wisconsin, Civil and Environmental Engineering, USA;
3University of Wisconsin, Comparative Biosciences, USA

Concern has been expressed that prions could enter wastewater treatment systems
through sewer and/or septic systems (e.g., necropsy laboratories, rural meat
processors, private game dressing) or through leachate from landfills that have
received TSE-contaminated material. Prions are highly resistant to degradation and
many disinfection procedures raising concern that they could survive conventional
wastewater treatment. Here, we report the results of experiments examining
the partitioning and survival of PrPSc during simulated wastewater treatment processes
including activated and mesophilic anaerobic sludge digestion. We establish that PrPSc
can be efficiently extracted from activated and anaerobic digester sludges with 1%
sodium dodecyl sulfate, 10% sodium undecyl sulfate, and 1% sodium N-lauryl
sarcosinate. Activated sludge digestion does not result in significant degradation of
PrPSc. The protein partitions strongly to the activated sludge solids and is
expected to enter biosolids treatment processes. A large fraction of PrPSc survived
simulated mesophilic anaerobic sludge digestion. Our results suggest that if
prions were to enter municipal waste water treatment systems, most of the agent
would partition to activated sludge solids, survive mesophilic anaerobic
digestion, and be present in treated biosolids. Land application of biosolids containing
prions could represent a route for their unintentional introduction into the environment.
Our results argue for excluding inputs of prions to municipal wastewater treatment
facilities that would result in unacceptable risk of prion disease transmission via
contaminated biosolids.


Chronic Wasting Disease in a Captive White-Tailed Deer Farm

Keane, D1; Barr, D1; Bochsler, P1; Hall, M2; Gidlewski, T3; O'Rourke, K4; Spraker, T5
1University of Wisconsin, USA; 2US Department of Agriculture, USA; 3US Department
of Agriculture, USA; 4USDA ARS-ADRU, Washington |State University, USA;
5Veterinary Diagnostic Laboratory, Colorado State University, USA

A white-tailed deer farm in Portage, Wisconsin, was depopulated in January 2006,
after chronic wasting disease (CWD) had been initially discovered on the property in
September 2002. Prior to the depopulation, a total of 22 positive animals had been
removed from the property: one in 2002, six in 2003, ten in 2004, four in 2005 and one
in 2006. At the time of depopulation a total of 76 animals remained: 47 females and 29
males. Age was assessed by visual examination of teeth at the time of death
and revealed 26 adult, 8 fawn and 42 yearling animals. The following tissues were
examined by immunohistochemistry for PrPCWD using Ab99/97.6.1: obex, tonsil,
retropharyngeal, submandibular, parotid, prescapular, axillary, inguinal, prefemoral and
popliteal lymph nodes, recto-anal mucosal tissue and eye. Seventy-nine percent of
animals (sixty) were found to be positive in at least one tissue; 49 were obex positive,
58 retropharyngeal positive, 56 tonsil positive, 48 recto-anal mucosal associated
lymphoid tissue positive and 4 animals were positive for PrPCWD in the retina. Prion
genotype was determined for all animals.


Quantifying the Species Barrier in Chronic Wasting Disease by a Novel in
vitro Conversion Assay

Li, L1; Coulthart, MB2; Balachandran, A3; Chakrabartty, A4; Cashman, NR1
1University of British Columbia, Brain Research Centre, Canada; 2Public
Health Agency of Canada, National Microbiology Laboratory, Canada; 3Animal Diseases
Research Institute, Canada Food Inspection Agency, National Reference Laboratory for
Scrapie and CWD, Canada; 4Ontario Cancer Institute and Department of Medical
Biophysics, University of Toronto, Canada

Background: Chronic wasting disease (CWD) is a transmissible spongiform
encephalopathy that can affect North American cervids (deer, elk, and
moose). Although the risk of CWD crossing the species barrier and causing human
disease is still unknown, however, definite bovine spongiform encephalopathy
(BSE) transmission to humans as variant CJD (vCJD), it would seem prudent to limit
the exposure of humans to CWD.

Aim: In view of the fact that BSE can be readily transmitted to non-bovid
species, it is important to establish the species susceptibility range of

Methods: In vitro conversion system was performed by incubation of prions
with normal brain homogenates as described before, and protease K (PK)
resistant PrP was determined by immunoblotting with 6H4 monoclonal prion antibody.

Results: Our results demonstrate that PrPC from cervids (including moose)
can be efficiently converted to a protease-resistant form by incubation with elk
CWD prions, presumably due to sequence and structural similarities between
these species. Interestingly, hamster shows a high conversion ratio by PrPCWD.
Moreover, partial denaturation of substrate PrPC can apparently overcome the
structural barriers between more distant species.

Conclusions: Our work correctly predicted the transmission of CWD to a wild
moose. We find a species barrier for prion protein conversion between cervids and
other species, however, this barrier might be overcome if the PrPC substrate
has been partially denatured in a cellular environment. Such an environment
might also promote CWD transmission to non-cervid species, *** including humans.
Acid/GdnHCl-treated brain PrPC was a superior substrate for the in vitro
conversion than PrPC treated at physiological pH. This has implications for
the process by which the prion protein is converted in disease.

Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil

Christopher J. Johnson1,2, Joel A. Pedersen3, Rick J. Chappell4, Debbie
McKenzie2, Judd M. Aiken1,2*

1 Program in Cellular and Molecular Biology, University of
Wisconsin-Madison, Madison, Wisconsin, United States of America, 2
Department of Comparative Biosciences, School of Veterinary Medicine,
University of Wisconsin-Madison, Madison, Wisconsin, United States of
America, 3 Department of Soil Science and Molecular and Environmental
Toxicology Center, University of Wisconsin-Madison, Madison, Wisconsin,
United States of America, 4 Biostatistics and Medical Informatics,
University of Wisconsin Medical School, Madison, Wisconsin, United States of

Soil may serve as an environmental reservoir for prion infectivity and
contribute to the horizontal transmission of prion diseases (transmissible
spongiform encephalopathies [TSEs]) of sheep, deer, and elk. TSE infectivity
can persist in soil for years, and we previously demonstrated that the
disease-associated form of the prion protein binds to soil particles and
prions adsorbed to the common soil mineral montmorillonite (Mte) retain
infectivity following intracerebral inoculation. Here, we assess the oral
infectivity of Mte- and soil-bound prions. We establish that prions bound to
Mte are orally bioavailable, and that, unexpectedly, binding to Mte
significantly enhances disease penetrance and reduces the incubation period
relative to unbound agent. Cox proportional hazards modeling revealed that
across the doses of TSE agent tested, Mte increased the effective infectious
titer by a factor of 680 relative to unbound agent. Oral exposure to
Mte-associated prions led to TSE development in experimental animals even at
doses too low to produce clinical symptoms in the absence of the mineral. We
tested the oral infectivity of prions bound to three whole soils differing
in texture, mineralogy, and organic carbon content and found soil- bound
prions to be orally infectious. Two of the three soils increased oral
transmission of disease, and the infectivity of agent bound to the third
organic carbon-rich soil was equivalent to that of unbound agent. Enhanced
transmissibility of soil-bound prions may explain the environmental spread
of some TSEs despite the presumably low levels shed into the environment.
Association of prions with inorganic microparticles represents a novel means
by which their oral transmission is enhanced relative to unbound agent.


Discussion These experiments address the critical question of whether soil
particle­bound prions are infectious by an environmentally relevant exposure
route, namely, oral ingestion. Oral infectivity of soil particle­bound
prions is a conditio sine qua non for soil to serve as an environmental
reservoir for TSE agent. The maintenance of infectivity and enhanced
transmissibility when TSE agent is bound to the common soil mineral Mte is
remarkable given the avidity of the PrPTSE­Mte interaction [22]. One might
expect the avid interaction of PrPTSE with Mte to result in the mineral
serving as a sink, rather than a reservoir, for TSE infectivity. Our results
demonstrate this may not be the case. Furthermore, sorption of prions to
complex whole soils did not diminish bioavailability, and in two of three
cases promoted disease transmission by the oral route of exposure. While
extrapolation of these results to environmental conditions must be made with
care, prion sorption to soil particles clearly has the potential to increase
disease transmission via the oral route and contribute to the maintenance of
TSE epizootics.

Two of three tested soils potentiated oral prion disease transmission. The
reason for increased oral transmissibility associated with some, but not
all, of the soils remains to be elucidated. One possibility is that
components responsible for enhancing oral transmissibility were present at
higher levels in the Elliot and Bluestem soils than in the Dodge soil. The
major difference between the Dodge soil and the other two soils was the
extremely high natural organic matter content of the former (34%, [22]). The
Dodge and Elliot soils contained similar levels of mixed-layer
illite/smectite, although the contribution of smectite layers was higher in
the Dodge soil (14%­16%, [22]). The organic matter present in the Dodge soil
may have obstructed access of PrPTSE to sorption sites on smectite (or other
mineral) surfaces.

The mechanism by which Mte or other soil components enhances the oral
transmissibility of particle-bound prions remains to be clarified.
Aluminosilicate minerals such as Mte do not provoke inflammation of the
intestinal lining [39]. Although such an effect is conceivable for whole
soils, soil ingestion is common in ruminants and other mammals [25]. Prion
binding to Mte or other soil components may partially protect PrPTSE from
denaturation or proteolysis in the digestive tract [22,40] allowing more
disease agent to be taken up from the gut than would otherwise be the case.
Adsorption of PrPTSE to soil or soil minerals may alter the aggregation
state of the protein, shifting the size distribution toward more infectious
prion protein particles, thereby increasing the specific titer (i.e.,
infectious units per mass of protein) [41]. In the intestine, PrPTSE
complexed with soil particles may be more readily sampled, endocytosed
(e.g., at Peyer's patches), or persorbed than unbound prions.
Aluminosilicate (as well as titanium dioxide, starch, and silica)
microparticles, similar in size to the Mte used in our experiments, readily
undergo endocytotic and persorptive uptake in the small intestine [42­44].
Enhanced translocation of the infectious agent from the gut lumen into the
body may be responsible for the observed increase in transmission

Survival analysis indicated that when bound to Mte, prions from both BH and
purified PrPTSE preparations were more orally infectious than unbound agent.
Mte addition influenced the effective titer of infected BH to a lesser
extent than purified PrPTSE. Several nonmutually exclusive factors may
explain this result: (1) other macromolecules present in BH (e.g., lipids,
nucleic acids, other proteins) compete with PrPTSE for Mte binding sites;
(2) prion protein is more aggregated in the purified PrPTSE preparation than
in BH [45], and sorption to Mte reduces PrPTSE aggregate size, increasing
specific titer [41]; and (3) sorption of macromolecules present in BH to Mte
influences mineral particle uptake in the gut by altering surface charge or
size, whereas the approximately 1,000-fold lower total protein concentration
in purified PrPTSE preparations did not produce this effect.

We previously showed that other inorganic microparticles (kaolinite and
silicon dioxide) also bind PrPTSE [22]. All three types of microparticles
are widely used food additives and are typically listed as bentonite (Mte),
kaolin (kaolinite), and silica (silicon dioxide). Microparticles are
increasingly included in Western diets. Dietary microparticles are typically
inert and considered safe for consumption by themselves, do not cause
inflammatory responses or other pathologies, even with chronic consumption,
and are often sampled in the gut and transferred from the intestinal lumen
to lymphoid tissue [39,46,47]. Our data suggest that the binding of PrPTSE
to dietary microparticles has the potential to enhance oral prion disease
transmission and warrants further investigation.

In conclusion, our results provide compelling support for the hypothesis
that soil serves as a biologically relevant reservoir of TSE infectivity.
Our data are intriguing in light of reports that naïve animals can contract
TSEs following exposure to presumably low doses of agent in the environment
[5,7­9]. We find that Mte enhances the likelihood of TSE manifestation in
cases that would otherwise remain subclinical (Figure 3B and 3C), and that
prions bound to soil are orally infectious (Figure 5). Our results
demonstrate that adsorption of TSE agent to inorganic microparticles and
certain soils alter transmission efficiency via the oral route of exposure.

snip...full text is here:

Chronic Wasting Disease (CWD) continues to spread
RONALD E. MCCALL | Thursday, September 27, 2007 at 12:30 am



CJD VOICE (voice for _all_ victims of human TSE)

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

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