September 4, 2003
Study: CWD easily spreads deer to deer
By ANDREW BRIDGES, Associated Press
Chronic wasting disease is transmitted more easily than previously thought, a finding that complicates efforts to curb the relative of mad cow disease as it spreads in populations of deer and elk, according to a new study.
Researchers who previously believed transmission from doe to fawn played an important role in its spread now say that's not the case. Instead, the contagious brain disease is "remarkably efficient" at spreading from animal to animal, new research shows.
The finding suggests it will be harder to control the fatal disease other than through the drastic thinning or eradication of infected herds, as has happened in parts of Wisconsin and Colorado.
"Unfortunately, that's what we're left with in the short term. In the long term, we hope something will come along," said Mike Miller, of the Colorado Division of Wildlife and co-author of the new study. Details appeared Wednesday in the journal Nature.
Researchers believe the disease spreads in deer and elk when they encounter infected feces or saliva. Concentrations of the animals, whether in the wild or in captivity, likely encourage its spread, as has the interstate shipment of infected animals, Miller said.
There is no evidence the disease infects either livestock or humans.
Miller and co-author Elizabeth Williams, of the University of Wyoming, Laramie, studied two populations of captive mule deer at a research center in Colorado. One set was born-to-captivity does that had contracted the disease. The second was born-in-the-wild deer free of the disease, but later captured and placed with the first group when 14 weeks old.
All of the animals in both groups eventually contracted the disease, which discounted the theory that maternal transmission was key to its spread, Miller said.
Judd Aiken, of the University of Wisconsin-Madison, said the study was important but its results were unsurprising.
"It provides further support of what's been apparent, that CWD is a contagious prion disease," Aiken said, referring to the modified proteins thought to cause the disease.
The disease affects the nervous system and is marked by weight loss, stumbling, tremors and lack of coordination. There is no cure.
Chronic wasting disease was first identified in 1967. Until several years ago, researchers thought the disease was restricted to animals living in a small region straddling Colorado and Wyoming.
It has since been found in Nebraska, Kansas, Montana, New Mexico, South Dakota, Wisconsin and the provinces of Alberta and Saskatchewan.
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<div class='quotetop'>QUOTE </div>I guess the author of that article didn't know, but it has also been found in northern Illinois.It has since been found in Nebraska, Kansas, Montana, New Mexico, South Dakota, Wisconsin and the provinces of Alberta and Saskatchewan.[/b]
White smoke, flying lead, and a whitetail downrange.
This article, while quite informative gives misleading information. Here is my response to the editor of Nature magazine
"Prion disease: Horizontal prion transmission in mule deer", by Miller and Williams, Nature 425, 35 - 36 (04 Sep 2003) presents misleading statements and a potentially erroneous interpretation of factual data. First, abnormal prions have never been demonstrated to be the casual agent of CWD or any other TSE disease. Second, of the two deer cohorts subject to analysis, cohort ("R") was born upon contaminated premises as shown by the author's own data. Cohort ("NR") was obtained from a reportedly CWD-free wild herd and was subjected to tonsil biopsies, to ostensibly detect any possible CWD. However, tonsil biopsies are not effective in finding CWD in young (3.5 month-old) fawns, hence there is no guarantee that the NR fawns are truly CWD-free.
Now, if one examines the author's Figure 2, the increasing disease incident rate and decreasing age-at-death rate could be more logically indicative of facility disease contamination, which had already been noted by the authors. Recently at a CWD Symposium sponsored by the USDA-APHIS and CSU (September 10 & 11th, 2003, Ft. Collins, CO) I asked just such a question of author Williams, who replied in the affirmative, but that contamination via feces, urine, salvia, or whatever else, is still animal to animal transmission hence, indirect horizontal transmission. However, to blindly equate horizontal direct animal to animal transmission, to indirect residual environmental contamination is grossly misleading and a disservice to readers.
If indeed, the FWRF pens are heavily contaminated with the unknown disease agent, then any attempted study of maternal verses horizontal transmission is rendered somewhat useless. The disease agent affecting a neo-natal could be sourced either from the mother at birth or from the contaminated environment into which the fawn was introduced. Note that the average death ages are virtually the same for each cohort (R=2.8 yr or 33.6 months verses NR = 3.1 yr or 37.2 months, but less the 3.5 month average age of NR fawns at pen introduction, or 33.7 months to death). One can then offer that the disease incubation period probably averages about 33 to 34 months and fawns were infected in an unknown manner, at or near the date they were introduced into the pens, either by birth or by translocation. Hence, with the pervasive and almost predictable infection and death rate in the research pens, maternal transmission still seems unlikely, direct horizontal transmission has not been proven, and abundant residual disease contamination is the conclusion of choice. With that, the author's deductions as to natural spread or commercial movement are rendered suspect.
The most important information in this article is that virtually ALL test subjects died between 33 and 34 months after being introduced into the pens via birth or translocation. That time period is the most direct evidence of the disease incubation period to date!
The CWD Foundation, Box 55 South Fork, CO 81154 tele: 719-657-0942