I find it interesting that mad cow disease can spread to people but chronic wasting does not. I know only a little about the complexity of prions; enough to know it's beyond my comprehension of any regular disease or even virus.
anyone know more?

Actually I believe the first known case of CWD in deer was one accidently released from a research center in northern Colorado in the 1960s. It is very hard to find reference to that article anymore, but here is one mentioning them first recognizing the disease then. I can't remember how they happened to release it, but the rest is history. It is now in a number of states, but more or less clustered within a couple hundred miles of that facility. That is primarily in southern Wyoming and northern Colorado.

http://www.ct.gov/dep/cwp/view.asp?a=2700&depNav_GID=1633&q=323412

I will post the article with a better history of the situation if I can find it.

Kreeger's cheerful optimism is unwarranted and more based on politics than science.
We know that CWD on elk farms is devastating. What we don't know is how rapidly it can move through a concentrated population, because game farm elk are all put down when it first shows up.
It is splitting hairs to cite differences between game farms and feedgrounds -- both bring elk into unnatural densities, more so than the normal "yarding" behavior in the winter.
If the feedgrounds aren't closed, we're in for an unparalleled disaster.

Unfortunately we don't really know how it is transmitted form place to place. Since it can infect rodents are they carried form place to place by winged predators? There is no doubt that it is devastating when it gets into an area, but the problem is how it gets there to begin with.

Currently, CWD has been found in at least 20 states, some much more distant than 100 miles from Laramie. Wisconsin whitetailed deer populations have been devastated by both the disease and the control measures. CWD has been transmitted from animal to animal by direct physical contact and by residual prions in the soil. Spread from place to place, ie. Oklahoma to Nebraska to Illinois, etc can almost always be traced to a truck, sometimes with a game farm logo on the door, most often in an illegal effort to provide a "trophy" hunt within an enclosure.

Thursday, April 03, 2008 A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41

A prion disease of cervids: Chronic wasting disease

Sigurdson CJ.

snip...

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

snip...

full text ;

http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html


P01.47

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 CWD.

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.

http://www.prion2007.com/pdf/PrionBookofAbstracts.pdf

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

Wednesday, July 9, 2008

10 people killed by new CJD-like disease USA



http://cjdmadcowbaseoct2007.blogspot.com/2008/06/novel-human-disease-with-abnormal-prion.html




The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.

http://www.cjdfoundation.org/fact.html



TSS