An Overview of Whirling Disease & its Spread

History in the U.S.	Effects in Colorado	Other Areas
Species Susceptibility	All is Not Lost	1998 Update

* DISCLAIMER *

REMEMBER: I'm a fly fishing guide - not a fisheries biologist. The information on this page has been compiled from several different sources and is intended only as a "Primer" for the "average" fisherman - who may not want to spend 20 or 30 hours sorting through all the available literature. If you want to dig deeper and see what the "experts" are saying in their own words, the "Whirling Disease Foundation" will get you started.

To answer the Second Most Common Question first: Whirling Disease does not harm other fish, animals or humans.
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Whirling disease, an infection of salmonid fishes caused by a microscopic parasite (not a bacteria or virus), is believed to be responsible for the decimation of wild trout populations in some of the most renowned trout streams in the Rocky Mountain West. The organism, Myxbolus cerebralis, attacks young salmonids, especially rainbow trout, before their cartilage hardens to bone, causing skeletal deformities and thus indirectly effecting some nerves (causing "blacktail"). M. cerebralis gets into the cartilage near a fish's organ of equilibrium and multiplies rapidly, pressuring the organ and causing the victim to swim erratically, losing its ability to forage or escape predators. The life-cycle of the parasite involves two stages and requires a separate host -- a Tubifex worm and trout or salmon, for each. In the rest of this text, Mc stands for Myxobolus cerebralis, the parasite, and WD stands for whirling disease. Mc can exist in the fish and not cause WD, so the two are not equivalent.

The lifecycle of M. cerebralis (starting at an arbitrary point) is something like this: Once in a fish, Mc destroys cartilage tissues and develops into microscopic, spherical "myxosporean" spores. These are released when the fish dies, is eaten, etc. This spore stage can live for many years in dried mud, survive temperatures to -20C, and other adverse conditions. Once in the mud or other debris, it is ingested by Tubifex tubifex, and grows inside the gut of the worm. It is expelled by the worm when Mc has developed into its "actinosporean" form. Described as looking like a grappling hook, this spore form is short-lived (3-4 days), but active. It "swims" freely in the water, and when it comes into contact with a fish, attempts to attach itself to (and penetrate) the skin. If successful, the actinospore releases its sporoplasm into the fish where they migrate through the spinal column and head, multiplying rapidly to as many as 500,000 per fish and attacking the cartilage that provides the structural integrity of the fish. When the sporoplasts have developed into the myxosporean form, the cycle is complete.

All ages of fish can become "infected" with Mc, but adult fish, with very little cartilage, are not adversely affected. Remember, the goal of a parasite is to be completely benign to the host(s). It is in very young fish that Mc causes the most damage because the young fish's skeleton is still mostly cartilage -- ossification of the material into bone takes place gradually during the first year of life. Brown trout, having been exposed for some long period of time to Mc (both originated in Europe), are quite resistant to Mc, and rarely develop WD. They do become carriers, but they have a strong immune response early in the infection stage and do not lose significant amounts of cartilage to Mc. Unfortunately, here in North America, Mc has "jumped hosts" to other trout. Rainbows seem to be the most susceptible, though other trout also can be severely affected.

History in the U.S.

Whirling Disease is thought to have spread from Europe, where it exists among the native brown trout and salmon as a benign infestation. It was first identified in the United States in the 1950s in shipments of frozen fish from a European fish importer. As a direct result of exotic species stocking it has subsequently been transferred into rainbow and cutthroat trout populations, where it proves lethal, and into those of other salmonids, where it is a lesser problem. Brown trout, possibly because they developed an immunity over the ages in Europe, are little affected by whirling disease. Rainbow and Cutthroat Trout, native to Pacific Coast waters, are among the most susceptible; its effects on Brook trout (actually a member of the Char family) are still uncertain, and Mackinaw (also Char) do not appear to become infected at all.

     According to the draft report for the February 1996 Whirling Disease Workshop, 21 states have reported the parasite in hatcheries or in the wild. West Coast fish health specialists and field biologists report very little evidence that whirling disease is affecting wild salmonid populations in Pacific Coast & Columbia River Basin draingages. Likewise, there seems to be no evidence of catastrophic declines in wild rainbow trout populations in the eastern or central United states. If this is the case, what puts wild trout populations in the intermountain West at risk? Certain conditions must be more conducive to an outbreak of the disease, and a massive research effort will be required to determine what those risk factors are.   Meanwhile, we must find ways to minimize the spread of this fish pathogen because clearly "the genie is out of the bottle." Like H.I.V. and nuclear power, this "genie" cannot be put back into the bottle. For now, containment and control are the only prudent management options available.
     Alternatively, we wonder if whirling disease has actually affected wild stream-dwelling salmonids in other U.S. regions and, if so, why it has rarely been documented. Many plausible explanations exist. Of all salmonids, rainbow trout are among the most susceptible to whirling disease. They also are very vulnerable to angler harvest. Outside the intermountain West, wild rainbow trout populations are not abundant. Even fewer have been managed with restrictive angling regulations that afford almost total protection from angler harvest for a decade or longer. More often than not, rainbow trout fishing in these regions is either sustained or supplemented by hatchery-raised trout. Without a detailed fish marking program, creel census, and intensive population monitoring to differentiate between the wild and stocked components, no real database exists on which to assess whether or not the disease could be affecting a wild stream-dwelling salmonid population. In the absence of such information, the stocking of hatchery-reared trout and the effects of angler harvest could mask any population-level effect on wild rainbow trout stocks caused by whirling disease.
     Without a disease sampling protocol that includes histological sectioning and quantitative testing for the presence of Mc spores, fisheries officials can only assume that the disease is not affecting their wild salmonid fisheries. Undetected, this disease can masquerade behind many disguises, including overwinter mortality, predation, habitat loss, water flow or temperature fluctuations, interspecific or intra-specific competition, or combinations of these factors.
      Continuing to take the "if-we-don't-look-we-won't-find-it" approach will only further delay discovering the real truth. In the intermountain West, the conventional wisdom that whirling disease is primarily a problem restricted to fish culture facilities has been proven wrong. Its effects on wild trout populations can be profound, even devastating. That is the new reality.
Barry Nehring, Colorado Division of Wildlife

Colorado

     Massive population declines of young trout were first noted in 1993 during a routine study of the Colorado River in Middle Park by DOW stream researcher Barry Nehring.   In September, he had found up to 12,000 young-of-the-year rainbow trout per river mile, along with some 10,000 brown-trout fry. By November, though the number of brown trout remained unchanged, the young rainbows had vanished. What's more, up to three separate age classes (all the fish hatched in a given year) of rainbows were missing. In essence, the river's wild fish were reproducing, as usual, but young fish were not surviving. Population data gathered from 1981 to 1986 showed no such pattern.
      Nehring found whirling disease spores among his sample population, and young fish exhibited the characteristic circular swimming motion from which the whirling disease draws its name. Whirling disease had entered the Colorado River system sometime in the late 1980s - after the five-year population study. During tests in 1995 Nehring reported catastrophic losses also among brook trout and some Colorado river cutthroat trout. Some sections of the Colorado River also show extreme impacts on brown trout as well. Similar declines (over 90% population losses in some instances) have subsequently been noted on the Lower Gunnison, Upper Gunnison, Poudre, South Platte and Rio Grande. A wild strain of rainbows introduced to the Arkansas River has shown no sign of new generations. Only Colorado's North Fork of Republican River and Animas River drainages show no incidence of Mc.
     Though other factors, including poisoning by nitrogen-gas bubbles on the Colorado, could be involved, whirling disease is the common thread among all the waters. While a cause-effect relationship cannot be proven with mathematic cerainty, the circumstantial evidence seems overwhelming: whirling disease or its complications (such as WD-weakened fish succumbing to other ailments) is the primary culprit in the disappearance of the state's wild rainbows
      Nehring urged reassessment of management policy. "When policy fails, try thinking," he concluded.

Montana

The big story in Montana is the Madison, between Hebgen Lake and Ennis Lake. They are seeing practically no Rainbow young-of-year surviving, and populations in much of that area are down 90%. The Madison is believed to have been infected for about six years. A serious study has shown that WD is in fact the cause. Below Ennis, WD has not established itself. This supports Colorado's evidence that large reservoirs stop or slow the downstream spread of Mc and WD.

There are many other areas infected as well, with some population losses as well. Montana had planned to further their no-hatchery policy (which is only on capable self-reproducing streams now) to capable lakes and reservoirs. They wanted to start with a strain of rainbow that has been self-sustaining for 15 yrs in Harrison Reservoir. This lake is now WD-positive, and its feeder streams (where spawning takes place) are also positive, and is seeing little Y-O-Y recruitment.

Utah

Utah has quite a few areas that are WD-positive. It started in '91 in a private hatchery in the Fremont River drainage. They took radical steps to eradicate it the upper Fremont by completely killing off the trout population and keeping it trout-free for three years. So far, it appears to be successful. Utah has very few naturally reproducing populations of trout, and no state hatcheries are infected.
Mc and WD is now being managed for control rather than eradication.

Idaho, Oregon, California, Nevada

There are some areas in each state that are WD-positive. No large population losses attributable to WD have been seen yet. California first found WD around 1960; it appears to have been introduced through frozen fish shipments (probable) independent of other infected areas in N. America. One drainage in the state had it, then tested negative for ten years, until last spring it tested positive again. This attests to the longevity and persistence of the disease.

Eastern U.S.

WD has been found in Michigan, Ohio, W. Virginia, Virginia, Pennsylvania, New York, New Jersey, Massachusetts, and possibly others. Most of these outbreaks were in hatcheries, though PA, NY, MI, and WV have had wild population infections. Mostly, they have not seen large population losses.

The World

WD has been found in New Zealand and South Africa. Possibly it has also been detected in Peru and Russia, though this is not confirmed.

Species Susceptibility

In conjunction with laboratory experiments at the University of California at Davis, the Bozeman Fish Technology Center has been conducting live box experiments on Willow and Blaine Spring creeks to measure the susceptibility of Montana's native and introduced salmonids to WD. Overall, the preliminary findings of this on-going research are disappointing. Yellowstone and westslope cutthroat trout and three strains of rainbows, including the Deschutes rainbow, are susceptible. Researchers wrongly theorized that the reported resistance of the Deschutes rainbow to Ceratomyxa shasta, a highly virulent WD-related parasite, might transfer to the WD organism. A "bullet proof" strain of rainbow trout has so far proved elusive. Experimental findings for bull trout and arctic grayling, although more promising, are based on too few fish to draw any firm conclusions at this time.

Colorado has tested various species and has seen interesting results. Tests with native cutthroat have been disappointing. Both Colorado River Cutts and Greenback Cutts appear to have as high a mortality as Rainbows, although Greenback seem to produce less spores. Colorado River Rainbows seem to fair slightly better than Tasmanian Rainbows, the strain that is used the most in hatcheries. Surprisingly, the Snake River Finespot (a.k.a. "Westslope") Cutt seemed to be virtually uninfected. Mc is rarely found in Snake River Cutts which are widely stocked in Colorado, although very little natural reproduction occurs. Pete Walker, Fish Pathologist, C.D.O.W. thus believes that the Snake River Cutthroat may be one of the most resistant of all trout species/subspecies to the disease. "This gives us cause for hope that there may be strains of rainbow trout out there that may be highly resistant to this organism". Contrary to other states' results, CO has seen hardly any infection in Kokanee. Blue Mesa kokanee (derived from Flathead lake, MT) run up to the Roaring Judy hatchery through an infected stream, into an infected hatchery, and yet almost no signs of Mc are found in the free-ranging fish.

Now for some good news:

Infection in trout is not always fatal. There is a long continuum of "disease", so we don't speak of all fish being infected (carrying) Mc as having whirling disease (WD). Many watersheds are "infected", but the trout populations are stable, reproducing, and rarely show signs of WD.

R.W. Hoffman, one of the world's foremost authorities on WD at the University of Munich's Institute of Zoology has found that hatchery trout treated with the drug Fumagillin were virtually immune to infection. If true, this might at least allow eggs from wild stocks to be fertilized in hatcheries and the fry "innoculated" before being returned to the wild. Dr. Hoffman reports that trout, once infected, are highly resistant to reinfection. They apparently develop antibodies which prevent further reinfection by more actinosporean Mc; so a fish that was lightly infected will survive, live an apparently normal life carrying the Mc spore, and release it upon death. Great progress could be made if the triggering mechanism that prevents reinfection could be isolated.

Of special interest are T. tubifex worms that appear to resist infection by the parasite. At the University of Montana, Missoula, parasitologist Bill Granath finds in preliminary studies that parasite DNA is detected in resistant worms 24 hours after spore infection, but is undetectable 4 days later. "It appears that parasite DNA enters the worm tissue, but doesn't develop," says Granath. These resistant worms fuel dreams about biological control: If they could displace susceptible worms in the environment, they could offer a potential natural control. Hendrick's laboratory also plans to investigate how resistant worms neutralize spores, and whether resistant genes can be passed to susceptible worms.
Granath's studies point to another potential weak spot in the parasite's life cycle: At 15 degrees Celsius, huge amounts of TAMs are released from the worms into the water, but at 5 degrees, few are released. This laboratory finding parallels field observations that hatchling rainbows, but not stream-sharing brown trout, contract whirling disease. Fish biologist Dick vincent of Montana Fish, Wildlife, and parks in Bozeman found that young Rainbows emerge in May, when waters are warm and filled with TAMs that bombard them. Young Brown trout emerge in March, when waters are colder and contain few TAMs. One implication is that selective pressures may eventually favor Rainbow trout that spawn earlier in colder waters.

! ! U P D A T E ! !

At the most recent Symposium in Fort Collins, Colorado in February of 1998, 200 scientists met to discuss the findings of 50 major whirling disease research projects. The amount of information gathered in the past four years is amazing. Although there is no apparent cure, there are several promising areas of investigation including the identification of genetically resistant species, interruption of the parasite's life cycle, and identification of the environmental and fish life history factors which allow the disease to prevail.
     The National Partnership on the Management of Wild and Native Cold Water Fisheries has awarded $535,000 in 1998 for 16 Whirling Disease research projects in four states. These projects will continue work on disease diagnosis, worm ecology, and fish life cycles that may offer some protection from the disease. This is the second year of grants by the Partnership, which is based at Montana State University and funded by the U.S. Fish and Wildlife Service.
    Bill Granath, a Professor and Director of the Program in Biochemistry & Microbiology at the University of Montana, has been awarded one of these grants to study parameters that determine development and production of the whirling disease parsite, Myxobolus cerebralis, in the aquatic worm, Tubifex tubifex. Granath (an avid fly-fisherman) believes that the weak link in the complex life cycle of M. cerebralis must be exploited in order to control it. -- comparable to other diseases caused by a parasite requiring an invertebrate host, such as malaria with the mosquito and lyme disease with the tick.
     This research will continue studies to determine the effect of temperature on the survival of recently discovered parasite "packets" from the worms; and the susceptibility of the worms collected from Montana drainages to the parasite. In-bred lines of resistant and susceptible Tubifex are being developed so means of resistance can be explored. Results will help assess the risk of certain rivers to the disease, and strategies for control.
New techniques to filter and quantify the triactinomyxon (TAM) actinospores from lake and stream water samples are helping to determine the seasonality and periodicity of TAM spore production and release. Progress has also been made to link this field filtration technique with the DNA-based polymerase chain reaction (PCR) technology to show that TAM spores from water samples collected in lakes and streams are in fact the TAM spores of M. cerebralis. These techniques have proven to be extremely useful in defining microhabitat "hotspots" of infection in Colorado.
A study of high elevation (over 10,000') lakes and streams aims to determine if the Mc parasite has become established in alpine and tundra habitats. Fish samples will be collected from up to 150 high elevation habitats.
Ongoing work on Colorado wild rainbows will determine whether they are actually developing resistance to Mc. The study compares the spore density and mortality rate of two groups of young-of-the-year fish spawned in the river -- one from wild adults reared prior to the onset of infection and the other from adults expose to the parasite as juveniles. Another study will determine the resistance to Mc of two groups of Snake River Cutthroat trout -- one with a 10-year history of previous exposure and one with no history of exposure.
And, immunologists from the University of California are collaborating with CDOW to investigate the antigen/antibody reaction to Mc in wild Rainbows in the Colorado River, and later, in Snake River Cutthroat.