Wednesday, February 1st, 2023
Wednesday, February 1st, 2023

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Commentary: Study sheds more light on possible source of CWD

Research continues to shed more light on the possible source of chronic wasting disease. (Stock Photo)

Chronic wasting disease is considered an existential threat to deer management and the user pay model of conservation.

Worse, increasing evidence suggests that the zoonotic potential (spread between people and animals) of this disease has been underestimated.

If you’re like me, you’ve probably wondered where CWD came from? All we know for certain is that it first appeared in northeastern Colorado and southeastern Wyoming in 1967.

Nonetheless, lack of data rarely prevents speculation. Some (mostly folks who want to minimize CWD effects or who distrust academics) suggest the disease is no big deal because “it’s always been around.” Others (not infrequently the animal-rights types) imply that CWD is some kind of curse caused by hunters’ selfish desires for deer overabundance.

In both cases, the answer is an emphatic “nope,” although high deer numbers and certain herd compositions undoubtedly facilitate spread by increasing the probability of animal-to-animal contact.

The point is that until recently, the origin story has been just that – a
story. The most plausible hypothesis has been that the disease “jumped”
from livestock to deer, although that possibility had never been tested.

It has been now.

A simple and straight-forward experiment performed by scientists at the
National Veterinary Services Laboratory, Case Western Reserve
University, and Iowa State has demonstrated that such a jump from sheep
to cervidae (deer or elk) likely occurred.

Basically, the researchers knew that CWD is very similar to scrapie (a fatal,
neurodegenerative disease of sheep and goats). And so, they tested the
obvious question of whether sheep or goat scrapie could infect
white-tailed deer.

Six-month-old fawns were given oral and intranasal infusions of brain homogenate from
scrapie-infected sheep and goats (i.e., syringes were used to drip
homogenate into the mouths and noses of the deer).

At 15.6 months, one of the deer treated with sheep scrapie homogenate was
injured and had to be euthanized. Subsequent examination of that
animal’s brain showed neurochemical evidence of disease.

The remaining deer inoculated with sheep scrapie eventually displayed
classical symptoms of neurodegenerative disease (e.g., hypersalivation,
grinding of the teeth, head tremors, and weight loss). Subsequent
post-mortem examination of brain and lymphoid tissues showed that all
had developed scrapie.

None of the deer inoculated with goat scrapie became ill and none showed neural changes consistent with infection.

Here are the two explanations (one substantially more likely than the other) for the origins of CWD.

Explanation 1: Range band sheep (large numbers) have been present on the landscape of
Colorado and Wyoming for more than 150 years. During that time, there
certainly were multiple opportunities for scrapie-infected sheep and
free-ranging deer to come into contact. This contact transmission is
precisely what led to the establishment of bovine tuberculosis in deer,
as well as brucellosis in Yellowstone bison.

The fly in the ointment, so-to-speak, is that CWD first was detected in
1967, even though range sheep had been present from the middle of the
19th century.

Explanation 2: During the 1960s, captive mule deer were held in sheep scrapie-contaminated
livestock pens on the Fort Collins campus of Colorado State University.
Once experiments were completed, at least some of these deer were
released in northeastern Colorado and southwestern Wyoming.

At the time, it was unknown that scrapie could affect deer and also that
scrapie could be transmitted environmentally (e.g., via contaminated
soil in the holding pens).

Likely, CWD in free-ranging deer originated by transmission of a scrapie variant we now know as CWD from the released captives.

The silver-lining, if there is one, might be that because susceptibility to
sheep scrapie is strongly influenced by genetics (e.g., black-faced
sheep are more resistant to scrapie infection than are white-faced
sheep), perhaps some deer will be genetically less susceptible as well.
There is some evidence to support this contention.

In theory, genetically more resistant deer could eventually become more
common than susceptible individuals, and while CWD wouldn’t disappear,
the overall percentage of infected deer might stabilize or decline.

In the meantime, eradication of this gradually spreading disease (or
successfully preventing it from eventually infecting new areas) is, most
likely, an unrealistic expectation.

Instead, managing the effects of CWD on hunter participation and taking steps to
suppress prevalence are a near universal requirement and will be from
now forward.

Russ Mason is the Michigan DNR executive in residence and adjunct professor
in Agriculture and Natural Resources at Michigan State University.

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