Study examines deaths of trout that eat alewife
Published 10:47 am Thursday, April 17, 2014
TRAVERSE CITY, Mich. — Subtle immune system changes may explain why some Great Lakes trout and salmon die from the lack of an essential vitamin after eating alewife, an important forage species, according to a scientific report released Wednesday.
Death from deficiency of thiamine, or Vitamin B1, is a primary obstacle to restoring lake trout, which were decimated by parasitic sea lamprey in the mid-1900s. It also hampers the stocking of chinook and coho salmon, popular sport fish native to the Pacific that were introduced into the Great Lakes in the 1960s.
Thiamine is needed for cell energy production and nerve function and is an antioxidant, meaning it can delay or prevent some types of cell damage.
Some fish hatch from eggs that were low in thiamine to start with, resulting in die-offs known as “early mortality syndrome.” Operators of Great Lakes trout and salmon hatcheries bathe young fish, or “fry,” in thiamine solutions to help them survive after being released to the wild.
But when they get large enough, they begin feasting on the alewife, an invasive fish believed to have reached the lakes through the Erie Canal and the Welland Canal that connects Lake Ontario and Lake Erie. Alewives carry an enzyme that destroys thiamine.
Scientists have worked for years to understand the mechanisms by which alewife consumption kills sport fish. In the new report, published in the journal Fish & Shellfish Immunology, researchers said lake trout deprived of thiamine were exhibiting immune system changes similar to those in humans with inflammatory diseases.
That suggests those fish have increased susceptibility to ailments such as bacterial kidney disease, a leading killer of chinook and coho, said Christopher Ottinger of the U.S. Geological Survey, lead author of the report. While the study focused specifically on lake trout, it’s likely that the findings apply to salmon as well, he said.
The discovery represents another step in piecing together the complex processes that can harm species playing central roles in Great Lakes food chains and the region’s $7 billion sport fishing industry.
“It becomes part of the picture about restoration of lake trout in the Great Lakes,” Ottinger said. “It helps managers look at their options and come up with solutions that best meet their needs.”
He acknowledged that the study provides no simple answers to the thiamine deficiency problem. Reducing the alewife population would deprive trout and salmon of an important food source.
A further complication is that thiamine deficiency levels can fluctuate from year to year, making it hard to determine proper water treatment levels, said Steve LaPan, head of the New York Department of Conservation’s fisheries section. Its Lake Ontario program applies thiamine treatments before the lake trout eggs hatch in hopes of catching the problem early.
Randy Claramunt, a fisheries research biologist with the Michigan Department of Natural Resources, said the study reinforces the importance of diversity in predator and prey species. Fisheries managers have made progress in restoring cisco, a native prey fish, in parts of the Great Lakes as an alternative to alewives.
Ironically, help also is coming from another invasive species — the round goby, which arrived in ship ballast in the 1990s. Not only does it gorge on pesky zebra and quagga mussels, but it provides a food source for trout and salmon.
Yet the round goby also has a downside. The mussels it eats are believed to carry botulism, which is killing loons and other aquatic birds that feed on gobies.
“All of this is reflective of the substantial changes happening in the Great Lakes from invasive species,” Claramunt said.