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Salmon smolts. Photo courtesy of Governor’s Salmon Recovery Office

Warming ocean conditions fuel viruses among species in the Salish Sea

As officials struggle to track and contain the outbreak of the novel coronavirus known as COVID-19, ecologists say widespread impacts from viruses and other pathogens are also a growing threat to the species of the Salish Sea ecosystem.

“We’re all especially impressed with how rapidly [COVID-19] emerged, the pace of its spread and how massively it has changed our world already,” said Dr. Drew Harvell of Cornell University at last month’s meeting of the American Association for the Advancement of Science in Seattle. “Infectious outbreaks of ocean organisms are also fast and impressive in scale but they are a lot harder to detect and track and see underneath the ocean.”

Harvell, who does much of her research at Friday Harbor Labs in Washington has studied the outbreaks of disease on ecologically important species such as starfish, corals and plants like seagrass. She is the author of the book “Ocean Outbreak” which looks at research on disease impacts in marine waters around the world, including the Salish Sea. She joined other scientists in a special session at the conference focusing on the impacts and responses to several diseases being studied in the region.

Harvell says that infectious disease outbreaks in the ocean are especially fueled by warmer water due to climate change. “Infectious agents are more virulent and grow faster at warmer temperatures,” she said.

Scientists are looking in particular at how these conditions might affect the region’s salmon populations. Dr. Kristina Miller of the Department of Fisheries and Oceans Canada who also spoke at the conference has been studying the emergence of a relative of COVID-19 that has been found in species such as Chinook and coho. Known as the pacific salmon nidovirus, it only occurs in salmon and there are no cases of its transference to humans.

“There are no examples of a virus being able to jump from a cold blooded vertebrate such as a salmon to a warm blooded human,” Miller said. “So we don’t have a zoonotic risk in terms of that kind of transmission. Our temperature profiles are way too different, and viruses actually are, most of them, somewhat specific to their hosts.”

Despite these differences, Miller hypothesizes that the nidovirus may also cause respiratory stress similar to COVID-19 in its salmon hosts and may be one factor in salmon declines, especially if it affects fish at the vulnerable smolt stage when they transition from freshwater to marine environments.

“What we find is that as salmon move from freshwater to the marine environment, the condition of the fish that are leaving these habitats makes a large difference in how well they are going to survive,” Miller said. “So if you already have a fish coming out of the river that is already stressed —  maybe it’s by disease or other factors — if you can mitigate those stressors and put out the healthiest possible fish to go into that marine environment… they will survive better.”

The nidovirus is just one of over 60 potential pathogens in salmon Miller and her colleagues identified in a study of thousands of wild, hatchery and farmed salmon. The true impact of such pathogens on salmon declines are not yet known, Miller said, owing to the difficulty of counting deceased fish. “The mere presence of a pathogen does not mean that a fish is diseased,” she said. “Disease is hard to study in wildlife when mortality is unobservable. Salmon in the ocean simply drop off in the water column, largely in the mouths of predators.”

But while counting deceased fish may be difficult, Miller and her colleagues are developing ecological models to estimate the level of mortality. “We are now employing this technology to explore the complex synergies between stress and disease and to identify regions along the coast where salmon are the most compromised,” she said. The model will combine data from studies of infectious diseases in salmon with factors such as ocean temperatures, which Miller called “the most significant driver of infection.”