Plant Detectives
On a routine sweep of her research territory, plant pathologist Cindy Ocamb stepped out of her car to survey a field of fertile Willamette Valley farmland. Stunted and dead turnip plants spread out before her. She pulled out a hand lens and stooped to inspect the leaf spots pocking the foliage. She had seen these symptoms only once before. They pointed to black leg, a potentially fatal, difficult-to-control fungal disease of turnips and their crucifer relatives—radishes, kale, cabbage, broccoli, and cauliflower—all grown in western Oregon for the international seed market and the expanding fresh vegetable market.
Ocamb, an associate professor in Oregon State University’s Department of Botany and Plant Pathology, collected samples from the turnip plants, then hurried to survey a field of canola, another crucifer relative. Again, the symptoms were significant. A trip further afield unearthed more evidence of the disease in commercial turnip fields. Ocamb cut the survey day short and headed to her laboratory on the Corvallis campus.
[caption caption="Melodie Putnam, director the OSU Plant Clinic, examines a blueberry plant for clues of disease. (Photo by Lynn Ketchum.)"]
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A look under a microscope confirmed her suspicions and raised more concerns. Downstairs in the OSU Plant Disease Clinic, she asked her colleague Maryna Serdai to examine a sample. Yes, she told Ocamb, it is black leg.
“Well,” thought Ocamb, “I won’t be taking sabbatical any time soon.”
Instead, throughout the spring of 2014, Ocamb trudged through muddy fields of crucifer vegetables and canola. In 43 of 60 sites she discovered black leg and two other diseases she’d not found in the past, including one never before reported in the U.S.
“Trouble comes in threes,” she says. “It certainly did this time.”
The two most important diseases— black leg and the newly discovered light leaf spot—distress the foliage of crucifer plants. Eventually, the disease reaches the stem and roots and the plant collapses. Through her investigation, Ocamb theorizes that at some time prior to 2013 seeds contaminated with black leg (Phoma lingam) and possibly light leaf spot (Cylindrosporium concentricum) were planted in an unknown field. How they got into the seed stream is a mystery, she says, because after a 1970s outbreak of black leg in the Midwest, testing and treatment became customary and the disease became rare. Ocamb guessed that the infected seed had come from a company that neglected to do routine testing and treatment.
When Ocamb arrived on the scene of that disease-infected turnip field, back in March 2014, she expected to find some plant mortality, the result of a particularly cold winter. “Some of the specialty seed growers had been talking about cabbage fields that had died out,” Ocamb remembered. “But when I saw all those dead plants, I was shocked.”
[caption caption="Michele Wiseman, a faculty research assistant, checks the roots of a blueberry plant for evidence of problems. (Photo by Lynn Ketchum.)"]
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Dead plants don’t often shock plant pathologists. But the discovery of the long-controlled black leg and a potentially more serious disease got her heart pounding. The consequences could be serious. “We’re one of only five places in the world to grow crucifer seed crops,” Ocamb noted. “It would have a huge impact if our production took a hit.”
Just one field planted with tainted seed can set off an outbreak. As some of those seeds germinate into diseased plants, they produce spores that splash from plant to plant during rain. Once spores pierce a leaf, the fungus takes hold and eventually kills the plant. The debris from dead plants harbors spores that can live for years and restart the cycle during the wet, cool weather of fall and spring. In those conditions, Ocamb estimates black leg and light leaf spot can move through a field within 2 months.
Through an ongoing experiment with graduate student Briana Claassen, Ocamb determined that the pathogen produced another form of spores, called ascospores, that blow on the wind. The two scientists placed uninfected plants in small pails hung alongside infected fields. After a week, they took the plants to a greenhouse and monitored them for 5 weeks. The black leg fungus showed up each time. Ocamb worries most about these windborne spores, which she thinks could be propelled up to 25 miles in all directions during storms.
Back in the lab at the Plant Disease Clinic, William Thomas, an OSU molecular and cellular biology scientist, examines the pathogens’ DNA. While black leg is easy to detect, light leaf spot can take an excruciating 2 months minimum to get accurate results. Thomas has developed a new molecular test that yields more comprehensive answers in less than 3 weeks, sometimes within days if the conditions are right.
“It’s like blood at a crime scene,” Ocamb says. “We collect it, run it, and match it to the victim.”
In 2015, cases continue to crop up, but the growing knowledge of control methods will lessen the death toll, says Ocamb with confidence. The key, she’s told growers, is to plow under or dispose of diseased residue, to deter windborne spores. Her research shows effective control also means spraying fall through spring while spores remain active.
“Management is not free and not easy,” she says, “but we can do it by getting everyone on the same page.” Ocamb thinks back to the drizzling day she came upon the scene of fields dying from disease. Now, she looks forward to closing the case.
[caption caption="Chris Mundt, a plant pathologist at Oregon State University, shows off a diseased leaf of wheat at a field day at OSU's Hyslop Farm. (Photo by Tiffany Woods.)"]
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West Nile virus. Foot-and-mouth disease. Ebola. These infectious diseases are no longer isolated occurrences. Environmental change and population mobility can ignite infectious diseases into global pandemics.
Chris Mundt is unraveling the mystery of how disease outbreaks become epidemics across the globe. “Our goal is to understand diseases that have the ability to disperse across very long distances,” said Mundt, a plant pathologist at Oregon State University and leader of a $2.5 million project to mitigate the potential for epidemics.
Diseases don’t always spread like a wave through a population. Sometimes they jump to distant locations, hitchhiking on an exposed traveller or infected animal. As pathogens move around a warming world, pandemic diseases increasingly threaten public health and global economies. And that’s the motivation for Mundt and an international team of scientists as they look for patterns in the dispersal of pathogens—whether virus, fungi, or bacteria, infecting people, plants, or animals.
For 15 years, Mundt and his OSU colleagues have been studying stripe rust, a fast-spreading fungal disease that infects wheat, one of the world’s most important food crops. The new study combines Mundt’s ongoing research with studies of other diseases, including two recent epidemics: foot-and-mouth disease in Britain and sudden oak death in California and Oregon. The researchers will also study earlier outbreaks of insect-borne viral diseases, such as West Nile, Rift Valley fever, and Japanese encephalitis.
These diseases have at least one thing in common: they develop rapidly and accelerate over time. If the life cycle of such a disease were graphed, the curve would appear steep at the beginning, with a long, fat tail accelerating through time. In contrast, the curve of a slower disease, like measles, would look more like a hill, up and down without a persistent, accelerating slope.
It’s been assumed, Mundt said, that most epidemics follow the same up-and-down pattern as measles. “But that wasn’t what I was seeing in stripe rust.” Instead, the outbreaks accelerated as they pushed out from the epicenter, and the larger the initial infection site, the faster the acceleration rate.
That’s the pattern in all these studies. The researchers will use findings from many disease outbreaks to test strategies for controlling epidemics, including eradicating host organisms around centers of infection. Mundt and his OSU team have experimented with eradication of wheat in a ring around a stripe-rust infection to halt its spread.
“There’s a lot of interest in how big that ring should be,” Mundt said. “Our research suggests that what matters more is how quickly you get on it, because of that accelerating disease front.”
The foot-and-mouth epidemic in Britain was halted by ring eradication, he said, but it was a drastic and controversial measure, resulting in the slaughter of some 4 million head of livestock. Foresters in southern Oregon also used ring eradication to slow the spread of sudden oak death, cutting and burning trees and shrubs around centers of infection.
“If what we’re seeing is correct,” Mundt said, “we need to increase early surveillance and respond rapidly to these fat-tail-pattern disease organisms, so we can safeguard the world’s health and food security.”
Mundt leads an international team of scientists on this 5-year project, funded by the U.S. Department of Agriculture’s National Institute of Food and Agriculture in association with the National Science Foundation, the National Institutes of Health, and the U.K.’s Biotechnology and Biological Services Research Council.