|
||||||||||||||||||
 |
From: TSS ()
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)gmail.com. By Jamie Svrcek Published June 8, 2007 I been beating the drums on this issue for 10 years, to no avail, thanks for http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&T=0&P=1165 http://www.ngpc.state.ne.us/cgi-bin/ultimatebb.cgi?ubb=get_topic;f=12;t=000488 http://www.pabucks.com/deer-hunting-forum/viewtopic.php?p=24420 http://www.michigan-sportsman.com/forum/showthread.php?t=186242 http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0704&L=sanet-mg&P=16289 http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0705&L=sanet-mg&T=0&P=22301 http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&D=1&F=P&P=8374 Singeltary, Sr et al. JAMA.2001; 285: 733-734. http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535 BRITISH MEDICAL JOURNAL JOURNAL OF NEUROLOGY MARCH 26, 2003 RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Email Terry S. Singeltary: flounder@wt.net 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? http://www.neurology.org/cgi/eletters/60/2/176#535 Tracking spongiform encephalopathies in North America Xavier Bosch Available online 29 July 2003. http://download.thelancet.com/pdfs/journals/1473-3099/PIIS1473309903007151.pdf 18 January 2007 - Draft minutes of the SEAC 95 meeting (426 KB) held on 64. A member noted that at the recent Neuroprion meeting, a study was Other work presented suggested that BSE and bovine amyloidotic http://www.seac.gov.uk/minutes/95.pdf Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE ***These results indicate that BASE is transmissible to humans and There is a growing number of human CJD cases, and they were presented He estimates that it may be up to 14 or 15 persons which display http://disc.server.com/Indices/236650.html kindest regards, Terry S. Singeltary Sr.
|
