Madison Crushing hopes that genetic barriers could slow the
spread of chronic wasting disease, a UW-Madison study suggests that
most deer are prone to the fatal ailment.
That’s the opinion of the study’s senior author and University
of Wisconsin professor of animal health and biomedical sciences,
Aiken, 47, is considered one of the nation’s leading authorities
on prion diseases. He has studied them since 1985, and has been at
UW-Madison since 1988.
“We don’t know the origin of CWD here in Wisconsin,” Aiken said
in a phone interview April 24, shortly before presenting the
study’s findings at a CWD symposium in Madison. “However, we do
know that this is a contagious prion disease, more contagious than
any of the other prion diseases out there.”
In the past year Aiken and other scientists examined DNA from
126 deer killed within the CWD-endemic region in south-central
Wisconsin, including 26 CWD-infected whitetails.
The team sequenced the prion protein gene known as PrP from the
DNA found in each deer’s cells. Although the normal function of the
PrP protein is not known, when an animal is exposed to CWD, the
protein converts to an infectious form.
Virtually all of the deer harbored a form of the gene found in
infected animals, Aiken said, indicating that between 86 and 96
percent of the deer in the region would be genetically susceptible
That means there’s little hope that Wisconsin’s wild deer herd
would over time and through natural attrition build a genetic
resistance to CWD, he said. It’s possible all deer are susceptible
to the disease, he said. Researchers could find no deer immune to
CWD, but because of limitations, they couldn’t say whether 100
percent of the deer could become infected.
Scientists have been limited by technologies that are available
to detect the abnormal protein, said Aiken, an Iola High School
graduate who earned his bachelor’s degree at UW-Stevens Point,
master’s degree at UW-LaCrosse and his Ph.D. in medical
biochemistry in Calgary.
“In the past, CWD research was not terribly well-funded,” he
said. “That’s changing now, and that should help.”
Aiken said he doesn’t believe environmental contamination a
popular alternative theory to abnormal prions is causing the
“I don’t think we need to invent a new source,” Aiken said. “I
would never say never, but given that, this is a contagious disease
that likely originated from Colorado or Wyoming outbreaks.”
The results of the UW study bolster the controversial strategy
of trying to eliminate the disease by sharply reducing deer numbers
in the CWD region.
The notion that some deer may have a genetic makeup that makes
them resistant to prion disease is the key argument for what some
believe would permit the disease to run its course in the wild deer
herd. Surviving animals, in theory, would form the basis of a herd
whose DNA would lack the genetic key to infection.
Aiken says the study effectively demolishes that argument.
“Statistically, we have a lot of confidence in our results,” he
Aiken says his group is continuing the study, sequencing the PrP
gene from additional deer from throughout the state and looking for
ways to diagnose the disease earlier.
UW researchers were recently awarded $5 million in federal funds
that will not only help in that effort, but also allow them to
study how prions react with the soil and whether other animals and
humans can be infected.
So far, scientists say there’s been no connection between
diseased venison and Creutzfeld Jacob Disease (CJD), the human
version of CWD. About one in every million people are afflicted
with CJD each year.
Aiken said he backs a national panel’s endorsement of the DNR’s
CWD plan, including a continued ban on deer baiting and
“Any infectious disease, if you concentrate animals, that’s
going to exacerbate the problem,” he said.
As for what had been called an eradication effort, Aiken agreed
shooting as many deer as possible in diseased areas is the best
“We really don’t have any other approach,” he said. “Increasing
the harvest will certainly slow the disease down. Most deer out
there are susceptible to the disease. These findings don’t mean
we’re not going to be able to stop the disease, but it tells us we
certainly can’t count on genetic barriers to slow it down.”