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CORVALLIS - When Jerri Bartholomew first heard that thousands of salmon, perhaps as many as 30,000, had died in a short time last week on a 40-mile stretch of the lower Klamath River, the Oregon State University microbiology professor was quick to come up with a suspect.

Sure enough, when the necropsy reports came back, one of the causes of the massive die-off was listed as Ceratomyxa shasta, a tiny parasite that Bartholomew first described the life cycle of in 1997, after 16 years on the trail in work supported in part by Oregon Sea Grant, the U.S. Fish and Wildlife Department and the Bonneville Power Administration.

As Bartholomew read the first news reports of the die-off, she was pretty sure that C. shasta was going to turn up as a culprit.

C. shasta kills fish by destroying the surface layer of the digestive tract. Two other causes have been identified as well, a bacterial disease called Columnaris, which attacks gill tissue, and ichthyopthirius multifiliis, or "ich," a parasitic infection causing a fish's own secretions to block its gills until it suffocates.

But while the three pathogens may have been the proximate cause of the fish deaths, there was another factor that may have been the actual trigger - the low water level in the Klamath River, biologists agree. The U.S. Bureau of Reclamation, which operates a dam at Upper Klamath Lake, had reduced the flow into the Klamath River to provide more irrigation water for farms in the Klamath basin. It did so despite warnings from biologists that the action could cause exactly this kind of problem.

C. Shasta and other such pathogens are almost always present in the waterways, but the returning salmon are able to survive long enough to get upstream and spawn. However, this summer's reduced flow made the river slower, shallower and warmer than usual.

"Those are all of the things parasites like," Bartholomew said. "The flow rate dictates the 'dose,' how many parasites or how many bacteria the fish encounter. The water temperature dictates how fast the pathogens multiply inside the fish."

As salmon began congregating in the shrunken river, awaiting a flow of water to signal the beginning of their journey upstream, their growing numbers crowded together, exposing them to the pathogens. Bartholomew said the resulting die-off, while not an absolutely foregone conclusion, was certainly no surprise.

The Bureau of Reclamation has responded to the die-off by increasing the flow from 760 cubic feet per second to 1,300 cubic feet per second. That may be enough to save any other fish that make it back into the river, but it's obviously too late for the salmon already dead.

"When you have adult fish that have returned from the ocean after four or five years out and there's that kind of investment and then you lose them, that's a tragedy," Bartholomew said.

Bartholomew first came to know C. shasta when, as a graduate student, she came to work in the OSU Fish Disease Lab with John Fryer, a pioneer in fish microbiology. There, the lab's staff was working to unravel a puzzling failure of an attempt to establish coastal steelhead runs in the Willamette River. Between 1966 and 1975 the project had raised and released more than a million smolts - and none of those fish ever returned as adults. In retrospect, scientists now agree they were probably killed by C. shasta. But how the parasite infected the fish, what happened to its spores after they left the fish, and its puzzling life cycle, were mysteries.

Researchers had learned that a related parasite, which causes whirling disease, goes through several life stages. They discovered that besides the stage that infects fish, the parasite spends part of its life in a completely different physical form, during which it infests a certain type of aquatic worm. Fryer thought C. shasta might have a similar life history. Fryer and his team began dredging debris from the bottom of infested rivers - rocks, muck, freshwater mussels - and putting it in laboratory tanks containing uninfected fish. Sure enough, those fish became infected with C. shasta.

"We knew the infectious stage of the parasite was present," Bartholomew recalled, "but we didn't know what it looked like or what its host was."

Then, in one of their tanks, Bartholomew and her colleagues discovered a tiny worm infected with spores that looked familiar. They began to gather the spores released by the worm, and feed them to fish in the lab. For three months they waited anxiously, checking daily to see if the fish were still alive. Finally, over Christmas break, Bartholomew discovered that the fish had died and that their guts were teeming with C. shasta spores.

"I never thought I could be excited by a fish dying," Bartholomew recalled. "But after 16 years of looking for the alternate host of C. shasta, I was really thrilled."

Through analysis of the organism's DNA, the OSU team was able to confirm that the spore found in the aquatic worm was, indeed, a life stage of the same organism that infests and kills fish. The discovery taught biologists an important lesson about the potential failings of hatchery production and the need to preserve native fish stocks that have built-in resistance to the pathogens that might be found in different streams. Bartholomew's work with DNA probes, meanwhile, provided biologists with an important new tool for learning about other organisms that cause disease in fish.

Bartholomew, now an assistant professor working in the lab, said she still works on C. shasta. Just last year she was called in to work with PGE on a huge die-off of juvenile chinook salmon in the Deschutes River.