Chronic Wasting Disease, a Tale of Woe

 

I recently returned from a mule deer hunt in Alberta. On the last day of the season, I was able to fill my tag with a nice buck, with help from my good friend and hunter host Glenn.

Unfortunately, I don’t know whether the deer will be edible.

In this part of Alberta, north of Medicine Hat and close to the Saskatchewan border, mule deer have a high incidence of chronic wasting disease, or CWD. Our friend Rob, who often hunts with us, has had his last two harvested mule deer from the same area (2017 and 2018) test +ve for CWD; he’s had a total of 3 +ve CWD mulie bucks over the past 5 years.

CWD is a prion disease thought to have originated from scrapie in sheep, but no one knows for sure. Prions are very weird, in that they are a ‘bent’ protein, not a virus or bacteria; so they are not a living entity in the classic sense. My friend Brian thinks they fall into the realm of ‘magic’, as they defy reason. There is no cure and once an animal is infected, the disease is always fatal. Apparently, the incubation period is a minimum of about a year, sometimes more than two years in mule deer, before clinical signs begin to develop (drooling, body tremors, loss of weight).

Worst of all, it seems you can’t get rid of CWD from the environment. It survives in soil and vegetation for upwards of a decade and even autoclaving won’t destroy it. Magic.

There is fear that as it becomes prevalent in a deer population, extinction of infected herds is a possibility. Game departments in a number of states and provinces are limiting movement of hunter harvested deer by enacting legislation that makes it unlawful to move around or import unprocessed carcasses. That means the animal must be de-boned and antlers on the skull plate cleaned. It’s hoped this reduces the rate of spread of the disease as these parts harbor most of the prions.

Where CWD is prevalent, or where there are worries it might show up, it’s either mandatory or recommended that the head of a harvested deer is submitted for testing, dependent on the jurisdiction and specific area the deer was harvested from.

It’s often said CWD is unlikely to jump the species barrier, but if it came from sheep, and is known to now occur in mule deer, white-tailed deer, elk, moose and caribou/reindeer, that claim doesn’t seem to hold a lot of water.

As of yet, it has not been diagnosed in humans, but the World Health Organization recommends against consumption of a CWD infected animal.

Trying to stop the spread and rate of infection of this disease is more than a challenge. There’s just not enough known about the disease.

For one, it seems old, mature mule deer bucks are much more likely to get infected than younger bucks or does of any age. In Alberta, whitetails on the same range as mulies have a very low rate of infection as well, although in other jurisdiction, for example in Wisconsin, whitetails in ‘hotspots’ do have high rates of infection. Free-ranging elk don’t seem to be particularly vulnerable to infection. Moose can become infected, but it’s rare. Reindeer in Norway were recently found with CWD (how did it get there? Previously, it had only been documented in the USA and Canada, at least as far as I can tell. CWD is not as yet a problem in Canadian or Alaskan caribou.

In elk, some specific genotypes don’t get the disease, but these animals, apparently, are rare in the population and exhibit other traits that make them undesirable. One such elk in a US compound has survived for years in a pen where all other elk that have been placed there over the years became infected and died. Her name is ‘Lucky’.

Other than trying to restrict movement of hunter harvested carcasses, the other method game agencies have used to try and stop the spread of the disease has been to de-populate deer in the area deer were been found to be infected (the Norwegians killed 2500 reindeer when they detected the disease in a couple of animals). This action seems to work in early stages, when only one or two animals have been found with CWD; but once it’s established, de-population is probably a lost cause. Killing all the deer to try and stop the disease from killing all the deer seems  . . . pointless, comes to mind.

In Alberta, the rumour is that mule deer management practices are going to change, perhaps as early as 2019, to try and contain the disease. Presently, mule deer are managed mostly through a draw, which directly limits harvest levels. This management practice has been in place for many years and resulted in Alberta substantially improving the overall quality of the buck harvest – a lot of bucks were able to live long enough to grow a big set of antlers.

But if it’s old bucks that are most likely to get and spread the disease, the thinking is that maybe it’s time to reduce the average age of mulie bucks. The easiest way to do that would seem to be to relax harvest restrictions by managing mule deer with a ‘General’ license; e.g., getting rid of the quota system and simply requiring hunters to buy a mule deer license/tag that’s valid during the open hunting season. More hunters, a higher harvest, fewer mule deer overall and far fewer old bucks.

That might work, except maybe not. In south-east Alberta, where CWD is most prevalent, there are large acreages that are more or less mule deer sanctuaries, and wouldn’t be affected by an easing of hunting restrictions. First off, there’s CFB Suffield; it’s 45,836 ha in size and right now, only open to limited elk hunting. There are also numerous large ranches (often these ranches are 10’s of thousands of acres in size) that either prohibit or severely restrict hunting, so any liberalization of hunting of mule deer would have little or no impact on those areas.

On the other hand, what are the options?

One thing for sure, more research effort is required. Unfortunately, because CWD impacts mostly on game animals and the hunting community – and hasn’t caused human illness or death (yet!!!) it’s a low priority for governments everywhere.

Still, there’s hope. Very recently, a bulletin from the Wildlife Society said “researchers found that high levels of major compounds in soil organic matter — humic acids — degrade CWD prions. When prions in soil were exposed to high concentrations of humic acids, researchers found lower levels of them. They also noted lower levels of infectivity in mice that were exposed to soil with higher levels of humic acids.” That’s good, and welcome news.

But more work is needed. Now.

In the meantime, I’ll be waiting for the results of testing on the mule deer I tagged.

Fingers crossed.

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Google photo

You are commenting using your Google account. Log Out /  Change )

Twitter picture

You are commenting using your Twitter account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s

%d bloggers like this: