Welcome, Guest
Username: Password: Remember me
  • Page:
  • 1

TOPIC:

Random thought Nov 08, 2016 2:03 pm #10183

  • BNature
  • BNature's Avatar Topic Author
  • Offline
  • Platinum Member
  • Platinum Member
  • Posts: 1559
  • Thank you received: 1484
It's common knowledge salmon and trout eggs in the hatcheries are treated with thiamine to prevent Early mortality syndrome - the result of a diet mostly consisting of alewives by their parents. Until gobies came into the mix and lakers depended almost totally on alewives, natural reproduction in Lake Michigan was near zero due to EMS.

So why don't the offspring king salmon spawning in Lake Michigan and Lake Huron tributaries (wild smolts) suffer from EMS?

Please Log in or Create an account to join the conversation.

Random thought Nov 10, 2016 5:00 pm #10187

  • Dirty
  • Dirty's Avatar
  • Offline
  • Administrator
  • Administrator
  • Posts: 5237
  • Thank you received: 1729
Interesting observation. I look forward to hearing some thoughts on this.
Boatless!

Please Log in or Create an account to join the conversation.

Random thought Nov 21, 2016 2:21 pm #10278

  • MC_angler
  • MC_angler's Avatar
  • Offline
  • Platinum Member
  • Platinum Member
  • Posts: 623
  • Thank you received: 1341
Actually in hatcheries prior to the early 90s, they didn't even routinely treat with thiamine because mortality was usually less than 20 or 30%. They just got more eggs than they needed to account for a small loss. EMS started getting worse after 1993, at which point they started treating every year in hatcheries.

Keep in mind that even though EMS can be a big problem, it doesn’t affect all smolts – you’re talking about 20-80% mortality, depending on the year. And it is variable, some years it is bad, some it is not. So they can still successfully reproduce even if EMS is an issue. It's not known if EMS is compensatory or additive mortality. I suspect that there is some compensatory factor to it (that is, if there is high mortality at the fry stage, it gives the ones that make it to parr stage an advantage because they have less competition from their peers for the same resources)

There was natural recruitment of all salmonines detected as soon as the early 70s. In the 80s the estimates were about a million chinook smolts produced annually... even up to 2 million. It's just that there were so many stocked fish that the wild fish were a very small proportion of the total population. Below is a graphic from a Michigan DNR research report summarizing salmon reproduction

This image is hidden for guests.
Please log in or register to see it.



The usual caveats apply: some of that is extrapolation between surveys, accurately estimating the number of smolts is difficult, nature is really variable, etc. But still - you can see that there was definite "non zero" reproduction as far back as the 70s and into the 80s, and really picking up steam thru the 90s, despite EMS being an issue.

By the 90s, estimates were between 2 and 3 million wild smolts produced annually. Those numbers rose considerably in the early 2000s, which is about the time massive ecosystem changes were happening (collapse of alewife in Huron, expansion of quaggas and gobies in both lakes, and a multitude of effects cascading thru the ecosystem). In the early 2000s, between 3 and 7 million smolts produced annually, with pretty big swings in some years due to environmental conditions. Obviously that is a higher proportion of wild fish than it was in the 80s, due to both increases in wild reproduction and concurrent decreases in stocking levels.

That's basically where we are today, although 2014 and 2015 were bad years due a combo of bad alewife yearclasses, drought, cold winter, and a depressed adult population in the lake.

Regarding the increase in natural reproduction over time, it’s likely that natural selection played a big role (chinooks with lower rates of Early Mortality Syndrome, and/or less susceptibility to thiaminase were more successful at reproducing, and evolution took it from there). The BKD die-offs may have played a role in accelerating that process. Certainly the massive ecosystem changes in the forage base probably played a role. Habitat improvements thru the 80s and 90s in Michigan rivers also helped, and the Clean Water Act probably was a big player too.

But in my mind, one of the biggest factors was the full colonization of rivers with excellent spawning habitat that were never stocked. Salmon were not stocked into all available spawning habitat. Tributaries of stocked rivers, and places where fish were never or infrequently stocked, like the Betsie River, the PM, a ton of other small Lake Michigan tribs, or a bunch of Canadian tribs to Lake Huron – it took a few generations to build up spawning populations of kings that strayed into these rivers. Once the rivers were colonized fully, they could start pumping out more and more smolts. So we likely didn’t “saturate” all available habitat until the 90s or maybe 2000s. But we’ve been at full saturation since then.
The following user(s) said Thank You: Dirty, Pikesmith

Please Log in or Create an account to join the conversation.

Random thought Nov 27, 2016 3:46 pm #10328

  • BNature
  • BNature's Avatar Topic Author
  • Offline
  • Platinum Member
  • Platinum Member
  • Posts: 1559
  • Thank you received: 1484
Thanks Ben. Didn't see this when you first posted. Some of it I knew or suspected just using common sense.

Devil's Advocate here: Are lakers more, less or similarly affected by the thiaminase ingested from eating alewives compared to king salmon?

Though you and the Michigan study showed ever expanding numbers of naturally produced kings from the beginning, during much of that period natural lake trout production was basically zero. My understanding the recent jump in natural reproduction of lakers happened only after gobies expanded and alewives declined in abundance - thus less thiaminase in the adult lakers and more reproduction.

Please Log in or Create an account to join the conversation.

Random thought Nov 28, 2016 8:51 am #10338

  • MC_angler
  • MC_angler's Avatar
  • Offline
  • Platinum Member
  • Platinum Member
  • Posts: 623
  • Thank you received: 1341
Lakers are probably more affected by thiaminase. The goby arrival is definitely a factor, as lakers incorporate more of them and fewer alewives. It's really hard to say with certainty just what factors are contributing and how much each factor is contributing. Because a lot of things are correlated, or even causated. Such as gobies, zebra mussels, quagga mussels, alewives, thiaminase, water clarity, plankton communities, and degree to which substrate is impacted by both live and dead mussels

Natural reproduction of lakers is much less understood than other salmonids, because they are for the most part spawing on big, deepwater reef complexes, which are very hard to sample and study compared to rivers

Please Log in or Create an account to join the conversation.

Random thought Nov 28, 2016 11:04 am #10339

  • Lickety-Split
  • Lickety-Split's Avatar
  • Offline
  • Platinum Member
  • Platinum Member
  • Posts: 2487
  • Thank you received: 1780
Isn't the other part of this, is the lower amount of alewife in the southern basin, means less predation on young newly hatched lake trout? Alewife eat young hatched lakers. I also read that with the jump in quagga and zebra mussels, that they(mussels) have consumed much of the toxins that was also killing the newly hatched lake trout. So the mussels have actually cleaned up parts of the lake that had interference with allowing the newly hatched lakers to survive. If this is true, then the parties that want natural lakers, may also not want to do away with the mussels as there is direct coralation between natural reproduction going up and the increase of mussels.
Lickety-Split

Life is not measured by the breaths you take
but by the moments that take your breath away

Please Log in or Create an account to join the conversation.

  • Page:
  • 1