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Righting the Rainbow

Photo: Courtesy of US Fish and Wildlife Service, Thomas L. Wellborn, Jr. DEADLY PARASITE: Myxobolus cerebralis causes whirling disease, a trout-killing infection that is devastating in some wild trout populations. In a Quonset hut dubbed the "parasite factory" on the University of California's sprawling Davis campus, the bed in a tankful of water is strewn with what looks like snippets of rusty thread: worms that harbor a deadly European parasite called Myxobolus cerebralis. It causes wh

By | October 14, 2002

Photo: Courtesy of US Fish and Wildlife Service, Thomas L. Wellborn, Jr.
 DEADLY PARASITE: Myxobolus cerebralis causes whirling disease, a trout-killing infection that is devastating in some wild trout populations.

In a Quonset hut dubbed the "parasite factory" on the University of California's sprawling Davis campus, the bed in a tankful of water is strewn with what looks like snippets of rusty thread: worms that harbor a deadly European parasite called Myxobolus cerebralis. It causes whirling disease, which has infected rainbow trout in 23 states in the United States, virtually wiping out the species in some of the West's best fishing waters. Researchers who have struggled for years to understand and control the problem are finally seeing the outlines take shape of a strategy to solve it. Through multifaceted collaborations, they have pieced together the highly complex life cycle of the parasite, including interactions with its two hosts, worms and fish. Moreover, investigators have begun to understand how environmental conditions affect these interactions, providing opportunities for effective interventions.

As is true with most parasites, containment rather than eradication is the objective. In that sense, whirling disease resembles human two-host diseases such as malaria or schistosomiasis. To characterize all ecological factors affecting parasite, worm, and fish remains a distant goal, just as reduction of the disease to undetectable levels through predictions and preemptive measures won't happen right away. But a principal step in that direction is now being taken. Based on the findings of laboratory and field studies--primarily in several western states, Virginia, and in Germany--researchers are beginning to develop risk assessment models that can identify conditions conducive to outbreaks. Indeed, the theme of the next annual whirling disease symposium, Feb. 6-7 in Seattle, is risk assessment.

Whirling disease is thought to have arrived in the 1950s with European frozen trout shipments to the eastern United States, although it didn't have a major effect on wild rainbow trout health, apparently because environmental conditions differed from those in western states. But in the mid-1990s, when the disease destroyed up to 90% of rainbows in Montana's famed Madison River and other fishing meccas, media coverage was heavy. The nonprofit Whirling Disease Foundation (WDF) was formed in Bozeman, Mont., and research money began to flow. WDF organizes the annual symposium and is a main funding source, along with the US Fish and Wildlife Service. Current federal funding is about $1 million (US) annually, with perhaps as much from state and private sources. Compared to research funding for human infectious disease, that's a pittance, but it's serious capital for fish health studies.

A visit to the University of California, Davis, Fish Health Laboratory, a hub of molecular work on the disease, reveals how much has been achieved. Lab head and infectious diseases professor Ron Hedrick stands alongside staff research associate Terry McDowell as they peer into buckets full of infected young trout. Some are black from tail to midsection, the spines of others bulge and curve, while others whirl in the water like dogs chasing their tails. Hedrick summarizes what has been discovered in recent years of the parasite's life cycle.

COMPLEX LIFE CYCLE Embedded in a stream, its initial form is that of a walnut-shaped spore just 10 microns in diameter that encases a living cell. After ingestion by the mud-loving Tubifex tubifex worm, the shell valves open, allowing the infectious sporoplasm to escape. It grows and changes into an anchor-shaped organism of 250 to 300 microns that is excreted by the worm and floats to the water's surface on three buoyant valves (hence, the name of this stage, triactinomyxon or TAM). These valves are secured to a central stalk, at the end of which, up to 64 cells are packed into the sporoplasm. At its tip, three cells transform into polar capsules, each of which can project a filament. To develop severe disease, a young fish passing through infected waters probably will contact thousands of TAMs that fire their filaments into the fish's skin. The sporoplasm enters through the hole and the rest of the structure falls away like a spent booster rocket, its delivery job done.

Within two hours, a replication cycle begins. Over the next several days, the cells migrate from the skin into peripheral nerves, eventually reaching the spinal cord and brain. About 20 days after initial infection, the parasites leave the nerves and begin attacking cartilage. Clinical signs begin at six weeks, as M. cerebralis degrades the cartilage with proteases and other extracellular enzymes, causing an inflammatory response from the fish. The inflammation and growing numbers of parasites combine to affect nerves that distribute pigment and influence swimming behavior, resulting in the characteristic black tail and whirling. Finally, encased spores form that are released after the fish's death, to restart the cycle.

The taxonomy of the phylum Myxozoa is under review, but recent genetic findings are expected to prompt its transfer from the protozoan to the metazoan subkingdom. Myxozoans share morphologic and functional characteristics with the stinging nematocysts that are so effective in jellyfish. M. cerebralis is among the most pathogenic of the 1300-plus phylum members. The annual cost to recreational fishing is difficult to pin down, because trout would have to be separated from other fish and an individual price placed on each hatchery-raised or wild trout. But WDF executive director Dave Kumlien believes that the figure is in the hundreds of millions and would rise precipitously if the disease ever spread to susceptible oceangoing species, such as steelhead and chinook salmon.1

Researchers are now investigating which fish are susceptible and why. For example, European brown trout are resistant, but many native American cutthroat trout strains are susceptible.2 Some species appear to somehow repel most TAMs, while others are infected but quell the disease through immune system responses. Rainbow trout, a Pacific coast species that was introduced to the Rocky Mountain States, come in hundreds of strains, but only one is known to be resistant. It was exported to Germany in the late 1800s, where it evolved a resistance that was announced at last year's WDF symposium by fish parasite specialist Mansour El-Matbouli.

His University of Munich group is researching numerous aspects of the disease, including vaccine development and immune responses in the resistant German strain compared to a susceptible rainbow strain. The possibility of introducing the German strain into hatchery-fed reservoirs is being avidly debated. Many scientists agree that wild trout waters should be protected from such introduction, for fear of affecting genetic diversity. Other fish species have not been examined yet as potential reservoirs of the disease.

Montana State University ecologist Billie Kerans says that another potential intervention, the introduction of a resistant T. tubifex strain from Canada, is unlikely in the near term, because less is known about the worm than the fish. One of her postdocs, Charlotte Rasmussen, is studying the genetic makeup of the worms along with Katherine Beauchamp in Hedrick's lab. The two women have assembled preliminary sequence data grouping the worms into at least three clades that vary tenfold in the amount of TAMs each produces.

In terms of risk assessment, Rasmussen says, "I think this will be a major factor, but it will be one of several." She cites the example of work by biologist Vicki Blazer at the National Fish Health Research Laboratory in Leetown, Va., showing increased TAM production at certain temperatures in a mud substrate compared to other substrates.

Photo: Courtesy of Whirling Disease Foundation
 DEADLY HOST: The Tubifex tubifex worm is home to the Myxobolus cerebralis.

ENVIRONMENTAL MANIPULATIONS With such information, risk assessment models can indicate which environmental controls in the wild are advisable under various conditions. For example, if risk of an outbreak is determined to be high on a dammed river, more water can be released. This will reduce the spores' silt habitat, lower temperatures below levels favored by the infectious TAM stage, and dilute the numbers of TAMs infecting each individual fish. If the high-risk stretch of water is undammed, signs can be posted warning fishermen to clean their boots and refrain from throwing fish heads back into the stream.

To assess risk with consistent accuracy requires yet more study of conditions that optimize the abundance and distribution of worms, their contact with large numbers of spores that originate from fish, and their proximity to young, susceptible fish. University of Montana parasitologist Bill Granath stresses that the behavior of the fish must not be overlooked. He notes that Montana's native cutthroat trout sometimes spawn and stay for several years in tributaries unfrequented by the parasite. By then, their skeletal system is mostly bone, providing little cartilage for M. cerebralis to feed on. Elsewhere, other cutthroat populations have the disease, leading Granath to research "point sources" or hot spots that could be cleaned up.

Effective control techniques such as filtration of TAMs and ultraviolet light treatment that kills them are already in use by hatcheries, but not until January will Colorado finally stop stocking infected trout in wild salmonid habitats. The state has accepted research findings that stocking infected fish even in waters known to carry the disease worsens the problem. David Nickum, executive director of Trout Unlimited's Colorado Council, notes that the state is also cutting back on river stocking in general. Montana, separated from Colorado by Wyoming, does not stock rivers.

This difference draws a wry comment on the complexities of parasitic disease from WDF scientific director Jerri Bartholomew, whose lab in the Fish Disease Research Center of Oregon State University principally studies myxosporeans. "I've always thought it interesting that two states that are managing fish so differently end up with the same problem," she says. "And I've never come up with an answer for that."

Steve Bunk (sbunk@the-scientist.com) is a contributing editor.

References
1. R.P. Hedrick et al., "Susceptibility of three species of anadromous salmonids to experimentally induced infections with Myxobolus cerebralis, the causative agent of whirling disease," Journal of Aquatic Animal Health, 13:43-50, 2001.

2. E. Wagner et al., "Comparison of susceptibility of five cutthroat trout strains to Myxobolus cerebralis infection," Journal of Aquatic Animal Health, 14:84-91, 2002.
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