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Disease and Parasites

A short while ago I had a call from Sarah Frankcom, a Biology student at Carleton University in Ottawa (my old Alma Mater). She had an assignment and wanted to talk about moose, mostly with respect to the area north of Kenora, in the vicinity of Grassy Narrows. Part of the assignment, or project, was to produce a Podcast.

So here it is.

Over the years, I’ve done a number of media interviews and given numerous presentation to various groups, so I was reasonably well-prepared for this. However, in listening to the tape, there’s a lot more that could be said.

But it is what it is.

I hope you find it at least somewhat informative

https://drive.google.com/file/d/1Uv7NMwF97imtqGq_LgXP7W2KygbA_1tp/view

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I haven’t blogged for many months. I’m sure most will understand when I say ‘there have been a myriad of reasons’ for my yap gap.

My last post was – posted – before the Covid madness had descended. The pandemic has changed every-bodies lives, everywhere in the world and continues to do so.

There’s a lot of talk about what the new normal is going to be, the one that emerges after all this period of change settles down, but who’s to know when that will be, or what it will look like. A phrase that I keep going back to is one about how the only constant in our lives is change. Every day is a new day, also comes to mind.

Except for a swath along the equator, most of the world sees constant, seasonal change. Even equatorial regions have alternating wet and dry seasons. No two seasons are ever exactly the same, although patterns and trends may be clearly evident.

Since my last posting, the ice and snow that covered our field, marsh and forest has melted away, replaced by many shades of mostly greens. A blue pond now compliments the summer skies. Goslings and ducklings have come to be and fawns now need be aware of bears as well as wolves. It’s summer!

Anyway, thoughts about the consistency of change that comes with the seasons is an underlying premise of this blog. Things are always different than they used to be, although trends are clearly evident..

The posting has been published. It’s my latest column in Ontario Out of Doors magazine. 

As per my practice, the posting is the unedited version of the column. I know the two are always a bit different, but I seldom compare the two and if I do, it’s only a very cursory look. Editors edit – that’s their job and most are good at it.

I’ll keep posting. There was a time when I posted about once a week – well, I can’t do that anymore.

Until next time, stay safe.

 

What Goes Up, Does Come Down

By: Bruce Ranta

I heard the hunter before I saw him. When we met on the trail, he looked at me, somewhat perplexed, then blurted out “They’re extinct!”

We were hunting moose – moose weren’t ‘extinct’, of course, but it did seem that way. Neither of us had seen a fresh track or any other sign of moose.

Unfortunately, the lack of moose didn’t surprise me. Moose on my stomping grounds close to my Kenora home had been on a steep decline for several years – and not just where I liked to hunt. Moose populations had been on a similar downhill slide in much of northwestern Ontario, neighboring Manitoba and Minnesota, as well as further afield, in places like Vermont and New Hampshire.

What was going on?

There were many theories. To sort it through, Dr. Murray Lankester, a parasitologist with Lakehead University and I analysed data pertaining to moose and deer in the Kenora area going back, in some cases, over 100 years. We concluded that several factors were driving forces behind moose (and deer) population fluctuations.[i]

For one, we found that both moose and deer populations surged in the aftermath of large, landscape scale disturbances, namely fires, large blowdowns, clear-cut logging and spruce budworm epidemics.  Deer abundance was also tied to winter severity – long, cold and snowy winters knocked deer down – short winters without much snow saw big upticks in deer numbers.

In the 1990s, deer and moose numbers swelled in tandem. Winters were mild and food was abundant. Even a bad winter in 1995 didn’t have much of an impact on deer – the woods were full of easy to reach and nutritious arboreal lichens growing on millions of balsam trees killed by a spruce budworm outbreak. The same thing had happened 40 years earlier.

When deer became super-abundant, moose numbers began to plummet. Brain worm appeared to be a factor. The parasite has no discernible impact on deer, but is deadly on moose. When deer densities get above 4-5 deer/km2, the disease becomes problematic to moose.

Deer densities rose to at least twice that level.

Exacerbating the problem was the weather – a series of wet summers made conditions ideal for terrestrial snails and slugs, the brainworm’s conduit for the disease.

High deer numbers also led to skyrocketing wolf numbers.

The quantity and quality of moose browse declined precipitously with a slowdown in logging and the maturing of burns and blowdowns.

In short order, the moose population crashed.

Deer eventually depleted the supply of arboreal lichens. Winters turned cold and snowy. Wolves were everywhere. Deer too, crashed.

Today, there aren’t a lot of moose or deer in much of the Kenora area (except in the city where deer are relatively safe from wolves and people feed them).

With deer numbers down, will the moose recover?

Maybe, although with only low levels of logging and no recent large forest fires or blowdowns, moose habitat is presently sub-optimal.

Deer have continued their downward spiral owing to a spate of snowy winters and continued predation by wolves. With few deer, wolves will eventually crash. Then, with at least a few mild winters – deer might stage a comeback. The next spruce budworm epidemic will help, but that’s still a few years off (budworm outbreaks occur about every 40 years).

The fact is, ups and downs are normal in many populations of wildlife.  Stable populations, especially in seasonal climates, are the rarity.

What happened in the Kenora area isn’t exactly why moose – or deer – numbers have gone up or down elsewhere. Still, there are parallels and commonalities.

Food availability is commonly linked to population changes, as is weather, the abundance of predators and human hunting pressure. Diseases are also problematic, especially during population peaks.

Across North America, some populations of barren ground caribou have recently shown dramatic declines. Although somewhat alarming, it’s not unprecedented. Northern herds have a history of spectacular ups and downs. In Alaska, the caribou population dropped by more than 50% in the late 1970’s. In Quebec/Labrador, the caribou population jumped from less than 200,000 in the late 70’s to around 1 million in just 20 years. They have recently plummeted to only a few thousand.

In winter, caribou eat lichens, a very slow-growing plant, almost exclusively. Although over-grazing lichens isn’t the only issue they face (wolves, hunting pressure, disease and parasites and the weather are also important), food does matter.

After being reduced to paltry numbers (and extirpated in eastern Canada), wild turkeys, aided by re-stocking and re-introductions, underwent a huge expansion in range occupancy and population. But in the USA, turkey numbers peaked about a decade ago, and have since declined – again, not unexpectedly – ‘new’ or reintroduced populations often flourish, subside, then have years of – you guessed it – ups and downs.

While wildlife population ups and downs can’t be curtailed, they can be managed.

As OFAH Wildlife Biologist Keith Munro says, “We really need to take a big picture approach to wildlife management. Rather than focusing on a single factor that may be affecting a wildlife population, we need to consider the whole system which includes, but is not limited to, harvest (both licenced and rights-based), predation, competition between species, diseases, parasites, and habitat”.

But no matter what we do, what goes up – does come down.

[i] To read the entire study, see Ranta, B., and M. W. Lankester. 2017. Moose and deer population trends in northwestern Ontario: a case history. Alces 53: 159–179. https://alcesjournal.org/index.php/alces/article/view/227)

 

When I began to write this, on April 8, 2019, the temperature outside was hovering just above the freezing mark and it had just begun a rain/snow mix. Snow still carpeted the ground, although there were bare patches under some of the conifers and on some south facing slopes. The ponds and lakes were still ice-locked, except where there’s current.

Now, three days later, not much has changed, except it’s clear and cold (-60 C this morning), rather than overcast with snow and rain.

Two geese showed up on the pond on April 5th and hung out most of the day, before leaving, but they have since returned, at least once. Last year, geese arrived on the pond the same date. I suspect these early arrivals are to do with claiming the pond as their own in an effort to build a nest and raise some young, something that has been a failure on this pond two years running. Maybe this year will be different and both geese and ducks can successfully hatch and rear some progeny.

The wolves whittled the deer down again this winter, but there are still a few around. The deer population, overall, is a shadow of what it was about 10 years ago and seems to still be on a downward trajectory. As I’ve said before, I don’t think deer herds here will recover until the next spruce budworm epidemic is well underway, something that as far as I know, hasn’t even started yet. Interestingly, I did see a deer chewing on some lichens the other day, but like deer, lichen abundance is minimal.

A couple of weeks ago I gave a presentation to the Canadian Institute of Forestry, Lake of the Woods Chapter, on Moose Emphasis Areas, or MEAs. Basically, MEAs are large patches of forest – e.g., 5-10 thousand hectares – where the forest managers try to coordinate the creation and maintenance of good to excellent moose habitat when carrying out forest operations, namely harvesting, renewal and maintenance of wood fibre. Dr. Vince Crichton – Doc Moose – gave a presentation on moose and moose management in general, and there were two other presentations by District Biologists as to how MEAs were actually being implemented in approved forest management plans.

I think there was a general consensus that good moose habitat is a key component of managing moose, but other factors, including predation, disease and human harvest, are also important. Unfortunately, all factors, not just moose habitat, are difficult to control.

For example, starting with moose habitat, successful planning and implementing MEAs require a skillful planning team. But that alone is not enough, as public input needs to be accommodated. In many areas, the benefits of MEAs might not be realized without restrictions on road access (you need roads to practice forestry, but roads also provide access to human hunters and other predators).Meaningful restrictions on road access can be difficult if not impossible, because the public simply won’t accept them.

And good habitat, even with road restrictions, might not be enough. Sometimes, predators can suppress prey (e.g., moose) populations – which in some circumstances might warrant predator control. But these days, any talk of predator control seems to be met with a great deal of derision. Governments everywhere – certainly here in Ontario – have pretty much tossed the option of predator control aside.

There’s not much that can be done about disease, but at least there have been, in this part of the country, harsher, more snowy winters of late, which has reduced (a) deer populations, which in turn has reduced the incidence of brain worm, a major moose killer, and (b) moose tick abundance. Moose ticks thrive when winters are short, but take a hit from early and late snow cover (moose die-offs from severe moose tick infestations are fairly common in some areas). Fewer deer also mean fewer wolves, so again, that’s a good thing. Bears are another story.

Human harvest can be controlled to some degree, but again, there are issues that probably should be addressed, but can’t, or aren’t. These include:

(a) there is little control over harvest by Aboriginals and Métis, who do not require licences to hunt and are generally not subject to road use restrictions. Some Aboriginal and Métis groups and communities have voluntarily agreed to moose harvest limits, but there are no enforcement mechanisms to ensure compliance.

(b) despite reductions in the number of adult tags available to licenced hunters in many Wildlife Management Units (e.g., in WMU 6 there was a single bull tag issued last year – to me – and I didn’t fill it), there is still an unrestricted, two week hunt for calf moose. That means anyone with a moose licence can hunt and harvest (one) calf moose in any WMU during the ‘open’ calf season.

(c) there seems to be a mis-guided desire to have a bull:cow ratio close to 50:50. Doc Moose presented evidence that bulls can be substantially fewer in number than cows and still ‘get the job done’. It seems patently ridiculous to lower the number of bull tags and increase the number of cow tags, especially in WMUs where moose are declining and below population targets.

(d) there is also evidence that shows younger bulls are less effective breeders than older bulls, yet in Ontario, there are no restrictions on what kind of bull a hunter can harvest with a bull tag. Cows are less responsive to the clumsier wooing of young bulls as compared to mature bulls and young bulls have both lower sperm counts and lower sperm quality, making conception less likely. In addition, in many WMUs, there has been a tendency to have an early bow season, to allow hunters to call in a bull to the close range a bow hunter requires. As such, bulls are harvested before or during the peak of the rut. Fewer old bulls and harvesting bulls immediately before or during the rut might still let all the cows be bred – at least in those WMUs with a reasonable moose population –  but breeding might not be concentrated during the prime estrus, around the end of September. As a result, calving can be spread out over a longer period the following spring, making it easier for predators that specialize in taking young calves (i.e., wolves and large bears), thus reducing recruitment.

Perhaps the biggest hurdle to moose management is cultural. In Ontario, moose management is not the pressing issue it used to be for the government, replaced with concerns such as the plight of species at risk and a desire to deal with climate change hysteria. The perceived indifference to moose by the government is exacerbated by the fact that many hunters have little faith in government actions or policies, resulting in a ‘I don’t give a damn’ attitude. So poaching and a general disregard for rules have, in my opinion, increased (and I’m far from alone in believing that).

While I’m not completely convinced things can’t be turned around, I’m not in the habit of looking at things through rose-coloured glasses, either. The problems are huge and not easily addressed.

MAFA2

Still, outside of moose (and deer) world, life is not all bad.  Spring is in the air, or at least it should be over the coming weeks. I do look forward to the return of the migratory birds and seeing the return of the colour green.

Plus many a BBQ, with a cold beverage in hand, are looming in my future. And that’s a very good thing.

 

 

Last fall, I went mule deer hunting in south-eastern Alberta, perhaps for the last time. As an explanation as to why this hunt might have been my last mule deer hunt there, I offer the following story:

I first applied for a mule deer tag in Alberta as a Canadian resident, which requires a resident guide (or as Alberta calls it, a hunter host), in 1998. I was finally drawn in 2002.

I was successful on that first hunt, as I have been each and every time I’ve been drawn. Generally, it takes three or four years of applying to get a tag. Although I apply in the same pool as resident Albertans, I have only been able to apply for an antlered mulie, which is A-okay by me. Over the years, I’ve taken some nice bucks.

The same year I was initially drawn for a tag, Alberta documented its first cast of chronic wasting disease (CWD), in a farmed elk.

From then, the infection rate grew quickly, and bad news it was, as one of the areas where the disease took hold was the area I was hunting (we stayed, and have continued to stay, at a ranch north of Medicine Hat. We’ve become good friends with the rancher family).

In an attempt to stop the disease, the Alberta Fish & Game did a cull in the area we hunt in 2006.

Since then, things have gotten much worse on the CWD front.

The first thing we noticed, after the cull, was that there were a lot fewer mule deer on the ranch.

A few years later, the deer numbers increased somewhat, but there was a new wrinkle – it became mandatory for hunters to drop off the heads of harvested deer to be tested for CWD. Then I couldn’t transport a deer back to Ontario unless it was de-boned and the skull cap and antlers cleaned.

Although CWD has not – yet – been known to infect humans, health agencies recommend animals known to be infected to not be consumed. So there was a waiting period after harvesting and butchering the deer before it was possible to enjoy eating it.

Still, our deer were, for a few years, always negative for CWD. That changed in, I think it was 2013, when Rob’s buck tested positive. Since then, Rob has had two more bucks test +ve and there have been others in our hunting party who have taken mulies that have come back as CWD +ve. Not good.

And it’s only getting worse. Check out this link for the history – and see the spread – of CWD in Alberta from the date of discovery to date https://www.alberta.ca/chronic-wasting-disease-history-in-alberta.aspx .

For a number of reasons, including the CWD issue, I hadn’t applied for a mule deer tag the last couple of years, even though I had enough priority points to draw one. But in 2018 Glenn and I decided I might as well apply and if drawn, do the hunt, as things were “unlikely to get better, and you never know – maybe the ‘hunter host’ system will change with a new government”. It’s possible that for a non-resident Canadian – like me – hunting mule deer with friends using the hunter host system might not be an option in the future.

Anyway, I applied, got drawn and did the hunt with Glenn. On the last day of the season, Dec. 1, I harvested a nice mature mulie buck.

A couple of days later, on the way home, we dropped off the head for CWD testing in Jenner. I took some of the choice cuts home to Ontario, put them in a freezer bag, labelled them, froze them and . . . waited for the results of the CWD tests.

As I already said, CWD is not known – as yet – to infect humans, but the World Health Organization and Fish & Game agencies caution against consuming an animal known to have CWD. CWD – so far specific to members of the Cervidae (deer) family, has been documented in the following species: white-tailed deer, mule deer, elk, moose and reindeer. CWD is one of a group of fatal diseases referred to as transmissible spongiform encephalopathies (TSEs). The group includes bovine spongiform encephalopathy or BSE (“mad cow disease”), which can be passed on to humans. In humans, this BSE is called variant Creutzfeldt-Jakob disease.

Basically, if you get variant Creutzfeldt-Jakob, your brain is eaten away and you eventually die.

While waiting for the results of the CWD test on my deer, an article appeared in Deer and Deer Hunting magazine (https://www.deeranddeerhunting.com/deer-scouting/deer-behavior/controversial-research-bacteria-not-prions-cause-cwd (a magazine I have written for) on CWD, reporting on a researcher (a Dr. Bastian) who thinks CWD may actually be the result of an infectious ‘super-bacteria’. It’s interesting – and offers new hope in terms of dealing with the disease in the future – but so far, no one has replicated Dr. Bastian’s research, so he’s out alone in the field with respect to his theory. I believe part of the ‘problem’ is that there are relatively few people doing basic research on CWD, so not many are even trying to replicate his results.

At any rate, I was still waiting when Rob forwarded me another article https://mountainjournal.org/story-482 that bluntly suggests CWD is bound to, at some point, infect humans. The paper also says that it’s really impossible to sterilize your hunting utensils if you’ve cleaned a CWD infected animal and that prions – the infective agent – are almost indestructible and could infect whatever your now contaminated utensils come in contact with. They (prions) have been found to be taken up by vegetation and can get picked up and spread around by vehicles. There’s a lot of very scary stuff in this article.

So here I am at home wondering if I’m going to have to throw out my hunting knife and meat saw. I have no idea what to do with the skull cap and antlers of my buck if it’s CWD+ve – seems to me it would be shedding prions wherever I put it –  and because I usually do the final cleaning by sanding off any remaining bits of dried flesh – all I can envisage is inhaling airborne CWD prions. All these thoughts tend to sicken me . . .

Then, On March 11, I get an email and a magic call from Alberta Environment and Parks . .  .my deer tested negative! I can eat the deer, keep my hunting knives and saws and clean and mount the antlers!

Great news indeed!

But I really don’t think I want to go through that kind of an ordeal again.

As CWD continues to spread, there’s a lot of thinking us big game hunters are going to have to do. Although a number of writers and others are working to try and minimize the dangers of CWD, I’m skeptical. This is a huge issue, possible a huge health issue, that could see lives lost.

Oh, and one more thing. If a deer gets CWD, that deer always dies, usually within 2-3 years. There are worries it will, eventually, decimate infected herds. Alarming population declines have already been documented in some CWD endemic areas in the USA.

CWD. It’s a bad thing.

 

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.

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Spring is in the air. Yesterday was a very nice, late winter’s day (actually, the 1st day of spring), although by evening the wind was howling, the temperature was plummeting and snowflakes were being blown around. But earlier, it had been a nice day.

It’s been a weird winter. For the first time since I’ve lived here – over 35 years – most of the winter saw the snow with a hard crust, the kind you can walk on. In fact, I’ve looked at snow records for this area that go back to 1955 and see no indication of a winter with similar snow conditions.

I don’t know how that’s going to play out for the local wildlife, but I’m inclined to think not too badly. During our daily walks with our dogs, we are regularly seeing snowshoe hares, ruffed grouse and deer. On the other hand, there aren’t near as many hares as there were earlier, a testament I’m sure to the hunting success of the lynx, marten and fox, the tracks of which we regularly encounter, but seldom see.

And while there remains a small herd of about 7 deer on our property, we note they are regularly harassed by wolves. We haven’t seen any wolves of late, but every few days their tracks show us they are still nearby. Neighbors have told us the wolves have killed at least a few deer in the past weeks near them. It’s a concern that in our drives away from town, we see few – very few – deer tracks. No signs of moose at all.

With so little big game, it’s hard to see that wolves didn’t suffer. Wolves can’t thrive on a diet of mice and hares. Research has shown that each wolf needs about one adult deer every 20 days over the course of winter just to survive. But wolves are, if anything, survivalists. I admit I’m amazed there are as many wolves as there are. When the deer population crashed four winters ago, I would have thought the wolf population would have followed suit no more than a year or two later.  Still, it’s only a matter of time.

Despite the recent melting, there’s still a covering of snow on the ground and it’s still dense enough to support one’s weight. Like I said, yesterday was nice; it was sunny for most of the day and the temperature got to about +80 C.  Last night it dipped to -150 C and isn’t supposed to get above the melting point again for another couple of days.  There’s a lot of ice on the local lakes – more than two feet on the lake where Lil and I went fishing yesterday, so ice-free days are still off a bit (yes, we did catch some fish. Tasty speckled trout, as a matter of fact).

On a gloomy note, I received a report last week on the state of chronic wasting disease (CWD) in North America, the prion, brain-wasting disease now found across wide swaths of North America that’s killing off white-tailed deer, mule deer, elk and even moose. CWD continues to spread and once established in an area, seems to be impossible to eliminate. Once an animal is infected, death always follows. Some of the models being used to predict the outcome of this plague suggest that local, perhaps widespread extinctions are possible, if not probable.

What a mess.

Oh well, it’s spring! No time to get depressed. Plenty of time for that later.

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I just returned from Brandon, where the 50th Annual North American Moose Conference and the 8th International Moose Symposium were combined and held. There were people from North America and Eurasia attending the meetings, but I only managed to intermingle for a short while; I was a one day attendant during a set of meetings, field trips and social events that lasted several days. I really enjoyed myself and it seemed to me that was the feeling that captured the general mood.

I heard several talks about moose and listening to those presentations was like music to my ears. I heard that as a species, moose seem to be faring well, although populations in some areas have declined precipitously. I live in one of those areas – northwestern Ontario – I was there to provide an overview of the factors driving moose and white-tailed deer populations in the Kenora District of Ontario.

I don’t think my presentation was quite as lucid as I had hoped and I know I made an error when I couldn’t see the labelling on one of the graphs I had inserted into the power point presentation. Unable to read the labels and the legend, I promptly got the deer and moose stats wrong. Oh well, that will be corrected during the final write-up and anyway,  I think the crowd got the gist of my presentation.

It’s still an emerging consensus, but it appears that in much of eastern North America’s moose range, moose populations are limited by the presence of a parasite called brain worm. In that eastern, wetter, more highly forested biome, the parasite is commonly found in populations of white-tailed deer, where it seems to affect deer minimally, if at all. However, when moose become infected with brain worm, the animal often dies.

In the western, drier and more open ranges of North America, there is little to no incidence of brain worm in deer or moose. The presence of brain worm seems to do a good job of helping to explain how moose populations are compromised by high populations of deer.

It seems that in the east, once deer densities exceed about 4 deer/km2, moose populations decline. When deer densities are low, rates of transmission of the parasite from deer to moose rarely occurs.

There’s a lot more to the stories on moose and deer dynamics, but one of the topics of interest is how moose recover from low densities. In western Manitoba, southern Saskatchewan and south-eastern Alberta – the Canadian prairies – the thinking is that moose populations have been on the rise coincident with a decline in the number of rural farmers and ranchers living on the landscape. There’s evidence that incidence of illegal, unregulated hunting wasn’t necessarily high, as moose populations were long-depressed in the prairies, but it didn’t take a lot of moose hunting to keep populations low. As people abandoned their homesteads, more and more moose managed to find refuge and survive. Today, moose populations in grain and cattle country are robust.

The eastern forest areas where moose have recently declined are the same areas where deer populations simultaneously surged. But recent winter of deep snow and cold have knocked deer populations back; if they stay low or decline further, moose populations may be poised to recover.

A growing concern is that where moose populations are lowest, recovery could be jeopardized by legal, but unregulated hunting (Aboriginals and Metis have the constitutional Right to hunt and fish; the present interpretation is this means the hunting of moose by some can be done at any time of the year and there are no seasons or bag limits on the harvest).

The moose harvest by such individuals may not have to be much to prevent severely depressed moose populations from recovery.

Unregulated hunting is certainly not the only issue regarding moose population (or other game species) recovery dynamics. But to help solve the puzzle as to how to effectively manage moose populations in particular, it’s a factor that needs a lot more attention than society at large has lately been willing to give it.

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We were out checking on our trail cams a few days ago we use to monitor our reintroduced elk herd (one was stolen – an $800 Reconyx; we reported the theft to the police, but it’s ‘not their top priority’). Didn’t see any live elk, moose, bear or wolves (however, quite a few were captured by the cameras) and only a couple of white-tails. I imagine the females of all species are busy with young and trying to be as secretive as possible, while the male deer are dealing with sensitive and fast growing antlers (the bull elk already have some pretty impressive growth!).

Of note, we did see several hen ruffed grouse and all of them had young. Didn’t see too many young poults, though; the ones we did see were smaller than a ping pong ball. But each hen did the ‘I’m hurt! I can’t fly! My wing is broken!’ and tried to lure me away from the young ‘uns. Some tried to scare me off with an ‘attack’, and al were quite vocal; hissing, mewing and doing other calls trying to distract me. I didn’t pester them for too long, just a minute or so while trying to get some photos of the ‘how to act wounded and lure the threat away from the babies’ routine.

One thing; there must have been great synchronicity in the hatch.  Synchronicity in hatching of birds, as well as the birth of ungulates, is thought to be good as it ‘swamps’ predators and helps reduce losses. For example, wolves and bears have an innate ability to know to look for newly born fawns and calves, but there is also an element of learning how and where to look which improves the effectiveness and efficiency of their search. So if the birthing season is prolonged, it gives predators a longer time period to hone their hunting skills to find newborn, good for predators but not so good for the prey. Once the newbies are a few weeks old, though, they have a much greater chance of escaping, as even a little fawn deer or calf knows how to run like the dickens or keep itself behind mom (e.g., a cow moose) as she fends off wolves or bears.

The best way to achieve a synchronized birth is to have a short, intense rut, when most of the females are bred in just a few days. A breeding cycle that drags on for many days, weeks, or even months, can be disastrous. And short, intense ruts are most likely to happen when there is a healthy population of prime, adult males around – they know how to woo the women.

It’s probably not near as complicated in grouse world, but the situation is likely similar. Older, male ruffed grouse might be better suitors than yearling; however, I suspect weather plays a more important role in grouse hatching success and synchronicity in nesting than behaviour. Early May – when the grouse were mating – was warm and dry. Late May and early June, hatching time for grouse, has been wetter and in a relative sense, cooler, which might not be great. Cool and wet weather can play havoc on new-born chicks; they often get pneumonia or other fatal ailments when the weather in inclement. Maybe next time we are out to check on our cameras we’ll see some more grouse families and get an idea on flock size. But at the moment, things are suggesting it could be a good fall for ruffies.

And given the ruffed grouse is one of the best tasting treats in the northern forest, that’s a good thing.

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Today I applied for a spring turkey hunting license in Michigan. Not sure how this will pan out, as there is still much to do before the hunt, if I do get to go.

Let’s look at the list: need to get drawn (apparently, the odds are good); need to renew my passport; need to fill out some forms to transport a firearm into the USA; and, I need to see if there are restrictions this year as to whether I can actually bring a turkey back into Canada from the states. Last year, a few friends hunted in the mid-west, were successful, but were not allowed to cross the border back into Canada with their birds. The problem was an outbreak of avian flu in the states – another wildlife health and disease issue. Anyway, it’s something I need to delve into and find out what the score is. No sense spending all that time and effort to travel and hunt and not be allowed to bring back a tasty bird (if I’m fortunate enough to harvest one!). On the other hand, I’ll have a chance to meet up with some old friends I haven’t seen in a while.

If I can’t harvest a bird that I can bring home from Michigan, I can still hunt in Ontario. Maybe I can do both, as the area I’m looking at going in Michigan isn’t far from Sault Ste. Marie, where there’s a healthy wild turkey population to the east, and a hunt on nearby St. Joseph’s Island. I’ll have to see how events unfold . . .

I really enjoy turkey hunting, but I find it somewhat distressing that a disease issue is once again a factor as to whether I can harvest, transport and consume my (potential) catch.

On my last post, I discussed chronic wasting disease and the fact there was a little bit of good news on that front. Not much, but a little. Despite the bad news about avian flu, most of the wild turkey story is good news. Growing up, there were no turkeys in Ontario; they were extirpated in the 1800’s. Today, turkey numbers in the province (progeny of wild birds captured from neighboring jurisdictions and then live released) are closing in on a 100,000.

There could be more. In northwestern Ontario, I think wild turkeys would do well in the agricultural areas around Fort Frances and Rainy River. After all, there are wild turkeys in parts of adjacent Manitoba, where the weather is similar, if not a bit more harsh. The problem is the government in Ontario, or at least some individuals, believe that because northwestern Ontario is outside the known, historical range of turkey, wild turkeys don’t belong. It’s a consideration which can make sense (one doesn’t want introductions of wildlife made willy nilly), but it’s not as if wild turkeys are exotic to North America.

What seems to have gotten the short shrift in this line of thinking is the fact that the agricultural lands of northwestern Ontario today bear little resemblance to what the landscape – and its associated faunal assemblage – looked like prior to European colonization. And outside of some sort of apocalyptic, catastrophic event(s), there’s no going back to the way it was. That’s nothing but a pipe dream, adhered to only by a small and radical fringe of extreme environmentalists.

However, it is what it is and with no close by Ontario turkeys, turkey hunting for me, at least for the foreseeable future, means going on a considerable hike.

All in all, it’s not necessarily a bad thing. It just could be better.

elk-4

About a month ago a good friend from Alberta forwarded me an article he found written by Angus M. Thuermer Jr., reporting on a a study on Chronic Wasting Disease (CWD) in Wyoming. CWD is an infectious disease known to occur in white-tailed deer, mule deer, moose and elk. It’s part of a family of diseases known as Transmissible Spongiform Encephalopathies (TSEs) where the infectious agent is thought to be a malformed protein known as a prion. Prions are not a bacteria nor are they a virus; they are a very strange and poorly understood entity. There is a human form of TSE called Creutzfeldt-Jakob Disease (CJD). To date, no humans are known to have contracted CJD from a CWD infected animal, although there is a variant CJD people have got from eating cattle infected with Bovine Spongiform Encephalopathy (BSE), another TSE. CWD is thought to have originated from Scrapie, the TSE sheep can be infected with.

CWD is a large and growing concern in North America because it’s a relatively new disease (the first known occurrence was documented in the latter part of the last century), it’s spreading and it’s wreaking havoc to deer herds in some areas. There’s no known cure for the dsease and once an animal contracts it the end result is always death. It’s spread into the area of Alberta where I hunt so it’s a particular concern for me and my hunting partners.

Thuermer Jr.’s article said that a study by a University of Wyoming doctoral student Melia DeVivo led her to believe the mule deer herd she was studying could potentially become extinct because of CWD in 41 years. The herd numbered some 14,000 in the early 2000s but had dwindled to half that in about a decade.

There was a lot of information in the article, but a couple of factoids were most interesting. One was that researchers found that deer with different genes react differently to CWD exposure; a key gene found with three combinations of alleles can make a deer up to 30 times more likely to be CWD-positive, depending on which genotype the deer is. That’s good news, because it suggests that over time, it’s possible if not probable that deer herds will become dominated by CWD resistant strains of deer (however, as the researchers point out, the strains that are resistant seem to be relatively rare, which might mean they might not be ‘good’ for the survival of deer in other ways; e.g., deer with the resistant strain might be bad mothers). Still, I think the news there are CWD resistant deer is very good news indeed.

The other good news is that studies have shown that free-ranging elk don’t seem to get high rates of CWD infection, unlike mule deer – and penned or ranched elk. No one seems to know why that is the case. Plus, in 2002, a penned elk herd of 39, purposely exposed to CWD, had all withered away and died or been put down within 10 years – except for a lone cow nicknamed Lucky. Apparently she’s still alive, doesn’t look sick, doesn’t test positive for CWD and has had a calf. So it looks like elk also have natural, genetic or other resistance to CWD.

Interestingly, the area I hunt in Alberta where CWD is problematic in mule deer, also has free-ranging elk (that’s one of them in the photograph) – that haven’t as yet, at least as far as I know, tested positive for CWD. That would seem to be consistent with what researchers have observed elsewhere.

To date, the results of the studies Theurmer Jr. reported on have not been published in refereed journals. That needs to happen; otherwise, these important findings risk being dismissed as mere speculation or musings.

CWD is a terrible disease likely to get much worse before it gets better. For a long time, all the news about CWD was bad. But now there at least appears to be a glimmer of hope that all will not be lost.

And that’s a good thing.