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From: TSS ()
Subject: Is Texas hunting coming to an impasse?
Date: June 8, 2007 at 8:02 am PST

Is Texas hunting coming to an impasse?

By Jamie Svrcek

Published June 8, 2007

Is the way that we hunt in Texas eventually leading to the downfall of the sport as we know it?

An article published in this month’s Field and Stream magazine gives new credibility to things that many have said about the way Texans hunt and points to the possibility of a ticking time bomb right under our noses.

That bomb comes in the form of chronic wasting disease, a spongiform encephalopathy that affects the cervid species. In laymen’s terms, it is the deer and elk version of mad cow disease.

As cited by “The quiet spread of CWD,” the said article in Field and Stream, by Jim Thornton, veterinarian Edward A. Hoover, a professor at Colorado State University and author of a forefront CWD study, points to the real danger of the disease being the way that it is spread — through the transmission of saliva, almost a surety under feeders and at mineral and salt licks.

While there are no known cases of CWD in Texas, you have to look a little deeper to see the potential danger to our deer herds. Captive herds are more likely to be infected than naturally free-ranging deer.

The problem is that, with the stocking practices that are in vogue on game ranches, there is also a huge lack of regulation to track where the animals are coming from.

Oftentimes, the ranchers who raise the deer that stock these game ranches fall in between the regulation of state livestock boards and state wildlife agencies and, just as often, lobby both sides of the fence to avoid the fees, regulation, documentation and other practices that cattlemen and herders must follow.

It’s easy to see that a couple of unscrupulous game managers and ranchers, driven by the potential money that goes along with the “trophy deer” hunt industry that has developed in the past few years, could easily ship deer from out of state and infect Texas herds.

And CWD is spreading. First discovered in Colorado in the 1960s, it has spread to 10 other states and not only in captive herds — it has also been found in wild deer.

According to a report from 2003 posted by Texas Parks and Wildlife, there is no way to test meat for CWD. The only way to test is by examination of brain and lymph-node tissue.

To further complicate this, the disease has been linked to nonliving proteins known as “prions”. These protein molecules do not die and can infect the ground where, say, an infected animal dies and decomposes.

It has been proven that, in captive herds, one infected animal can infect up to 80 percent of the rest of the herd.

It makes sense that, with this looming on the horizon, maybe it is time to change the course of hunting in Texas.

The notion of hunting feeders, especially with the present agri-techonology available for food plots, makes them obsolete.

Besides, it has been proven that deer benefit from year-round nutrition programs, both in terms of health and horn development.

That leaves one issue, high fencing. This is one issue that you either love or hate.

What many see is the classic case of a few benefiting at the possible expense of the rest of the state’s hunters.

Those who hunt fenced land point to the ease with which herds can be managed and the decreased possibility of poaching.

Outfitters like fencing because it makes it easier to put high-paying clients on the deer that they “want.”

From a biological standpoint, it seems to come down to one thing; when a land- or lease-owner puts up high fencing, he has just captured wild animals and in effect “domesticated” them.

It is an ethics issue after that for the most part, although for many it’s strictly a money issue, until you factor in problems such as CWD.

With it proven that captive herds are more susceptible to contracting CWD, wouldn’t it be easier to protect the deer population without adding these problems on top of it?

Until next week, I’ll see you “Out There.”

Jamie Svrcek is the outdoors columnist for The Daily News. Contact him at jamiesvrcek(at)

----- Original Message -----
From: "Terry S. Singeltary Sr."
Cc: <>; <>
Sent: Friday, June 08, 2007 10:11 AM
Subject: re-Is Texas hunting coming to an impasse? CWD

Is Texas hunting coming to an impasse?

By Jamie Svrcek

Published June 8, 2007


I been beating the drums on this issue for 10 years, to no avail, thanks for
bringing it to light. cwd is a small part of a much larger problem i.e. TSEs
in all species, all of which have been rendered and fed back to animals for
human and animal consumption. please take the time to read over this
material, cwd has been at our doorsteps for years, but is it here? see for
yourself, just how close it is. ...

Re: Colorado Surveillance Program for Chronic Wasting Disease
Transmission to Humans (TWO SUSPECT CASES)

----- Original Message -----
From: "Terry S. Singeltary Sr." <[log in to unmask]>
To: <[log in to unmask]>
Sent: Saturday, December 23, 2006 1:47 PM
Subject: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low testing
sampling figures -- what gives TAHC ???;f=12;t=000488

Deer-scent ban aims to prevent wasting disease

Date: Fri, 25 May 2007 14:00:44 -0500
From: "Terry S. Singeltary Sr."
Subject: MAD COW USA and what we feed our food-production animals THE

Date: Mon, 21 May 2007 16:24:15 -0500
From: "Terry S. Singeltary Sr."
Subject: May 2007 Update on Feed Enforcement Activities to Limit the
Spread of BSE

Date: Tue, 16 Jan 2007 15:56:42 -0600
From: "Terry S. Singeltary Sr."

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.



vCJD in the USA * BSE in U.S.
15 November 1999


U.S. Scientist should be concerned with a CJD epidemic in the U.S., as
2 January 2000


MARCH 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

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?

Copyright © 2003 Published by Elsevier Ltd.

Tracking spongiform encephalopathies in North America

Xavier Bosch

Available online 29 July 2003.

Volume 3, Issue 8, August 2003, Page 463

“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.”


18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on
7 December 2006 are now available.


64. A member noted that at the recent Neuroprion meeting, a study was
presented showing that in transgenic mice BSE passaged in sheep may be
more virulent and infectious to a wider range of species than bovine
derived BSE.

Other work presented suggested that BSE and bovine amyloidotic
spongiform encephalopathy (BASE) MAY BE RELATED. A mutation had been
identified in the prion protein gene in an AMERICAN BASE CASE THAT WAS


3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse

Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case
Western Reserve University

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE
strain discovered recently in Italy, and similar or different atypical
BSE cases were also reported in other countries. The infectivity and
phenotypes of these atypical BSE strains in humans are unknown. In
collaboration with Pierluigi Gambetti, as well as Maria Caramelli and
her co-workers, we have inoculated transgenic mice expressing human
prion protein with brain homogenates from BASE or BSE infected cattle.
Our data shows that about half of the BASE-inoculated mice became
infected with an average incubation time of about 19 months; in
contrast, none of the BSE-inoculated mice appear to be infected after
more than 2 years.

***These results indicate that BASE is transmissible to humans and
suggest that BASE is more virulent than classical BSE in humans.***

6:30 Close of Day One

1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype of 'UNKNOWN'
strain growing. ...

There is a growing number of human CJD cases, and they were presented
last week in San Francisco by Luigi Gambatti(?) from his CJD
surveillance collection.

He estimates that it may be up to 14 or 15 persons which display
selectively SPRPSC and practically no detected RPRPSC proteins.


kindest regards,

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

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