Myxobolus cerebralis Hofer, 1903

Common Name: Myxosporean parasite, salmonid whirling disease

Synonyms and Other Names:

Myxosoma cerebralis




Dr. Thomas L. Wellborn, Jr. via U.S. Fish and Wildlife ServiceCopyright Info

Identification: M. cerebralis occurs in two stages. In one stage it has a myxospore form that contains a polar filament for injection of the cell contents (containing a binucleate infective germ cell) into the epithelial cells of the intestine of a host oligochaete (Tubifex tubifex). In the other stage it has a triactinomyxon (TAM) spore form that also is equipped with a polar filament for attachment to the epithelium of a salmonid host. In general, spores are oval, frequently asymmetrical, and exhibit 5 or 6 irregular coils in the polar filament (Mills et al. 1993; Gilbert and Granath 2003; Lom and Hoffman 2003; Kallert et al. 2005).            

In infected salmonids, the disease caused by M. cerebralis can result in whirling behavior or tail-chasing; damage to the central nervous system and organs of equilibrium; lesions in the skull, gills, and vertebrae; and sometimes mortality (Mills et al. 1993; Crawford 2001; Gilbert and Granath 2003; Krueger et al. 2006).


Size: M. cerebralis spores are around 7.5–10 μm in length (Lom and Hoffman 2003; Krueger et al. 2006).


Native Range: Unknown. However, M. cerebralis is a common European parasite of Brown Trout (Salmo trutta) and could have evolved with this host species, which is generally asymptomatic to infection. This association could have originated in Central Europe (Crawford 2001; Gilbert and Granath 2003; Krueger et al. 2006).


Map Key
This map only depicts Great Lakes introductions.

 
Great Lakes Nonindigenous Occurrences: M. cerebralis was recorded for the first time in 1968 in an Ohio aquaculture operation within the Lake Erie drainage. It may have been present in the Great Lakes system since the 1950s. It has been recorded primarily from aquaculture facilities, or waters in the immediate vicinity of such operations, in the Lakes Erie, Ontario, and Michigan drainages, but also in the wild in tributaries of Lakes Huron and Superior (Mills et al. 1993; Whirling Disease Initiative 1997-1998; Crawford 2001; Great Lakes Fishery Commission 2001). In 1998 M. cerebralis was also discovered in Yellowstone Lake, Wyoming (Tronstad et al. 2010).


Table 1. Great Lakes region nonindigenous occurrences, the earliest and latest observations in each state/province, and the tally and names of HUCs with observations†. Names and dates are hyperlinked to their relevant specimen records. The list of references for all nonindigenous occurrences of Myxobolus cerebralis are found here.

State/ProvinceYear of earliest observationYear of last observationTotal HUCs with observations†HUCs with observations†
Michigan197020036Au Gres-Rifle; Au Sable; Boardman-Charlevoix; Cheboygan; Lake Huron; Manistee
Minnesota197019701Lake Superior
New York197019881Lake Ontario
Ohio196819681Lake Erie
Wisconsin199819981St. Louis

Table last updated 5/25/2018

† Populations may not be currently present.


Ecology: M. cerebralis is the causal agent of salmonid whirling disease. Rainbow Trout (Oncorhynchus mykiss) is particularly susceptible to this pathogen. The following species are susceptible but generally considered less so than Rainbow Trout: Sockeye Salmon (Oncorhynchus nerka), Golden Trout (O. aguabonita), Cutthroat Trout (O. clarki), Brook Trout (S. fontinalis), Atlantic Salmon (Salmo salar), Bull Trout (Salvelinus confluentus), and Chinook Salmon (Oncorhynchus tshawytscha). Brown Trout (S. trutta) is susceptible but infections are usually asymptomatic. Lake Trout (Salvelinus namaycush) is not susceptible to infection (Bartholomew et al. 2003; Gilbert and Granath 2003; Sollid et al. 2003; Blazer et al. 2004; Krueger et al. 2006).            

M. cerebralis has an obligate host: the oligochaete T. tubifex. Different strains of this species are susceptible to infection by M. cerebralis while others are not. TAMs develop in T. tubifex via asexual and sexual reproduction, requiring a total of 3 months in the region between the epithelial cells of the oligochaete’s intestine to reach maturity. They are then released into the water column and must infect their salmonid hosts within around 1–15 days. Both mechanical and chemical mucus-derived signals trigger their discharge. Upon discharge at the epidermis of the fish, the sporoplasm, containing a group of infective germ cells, is injected into the host. The germ cells then move into the nervous system, reproducing and eventually moving to the cartilage. Development in the fish host is asexual and occurs in inter- and intra-cellular spaces, requiring around 3 months for myxospore formation. Myxospores can be passed to another fish at this point if the first host is ingested by a predator. If this is the case, they will pass out in the second host’s feces to settle in the sediments. Otherwise, the spores remain in the first fish host’s tissue upon mortality and eventually end up in the sediments as the carcass decays. Myxospores can survive temperatures of -20°C. They are then taken up from the sediments by feeding T. tubifex and the lifecycle begins again (El-Matbouli et al. 1999; Gilbert and Granath 2003; Kallert et al. 2005; Elwell et al. 2006; Kaeser et al. 2006; Krueger et al. 2006).

The severity of infection in salmonids may be correlated with water temperature and water conductivity. Temperatures from 5–17°C are best for TAM production while temperatures of >20°C are inhibitive. Depending on the strain of T. tubifex hosting TAMs, ideal temperature for development can vary. Finer sediments also may hold spores better than more coarse sediments. Moreover, finer sediments and slower moving waters are ideal habitat for T. tubifex and thus may favor higher infection rates in salmonids. Finally, larger and older rainbow trout (at least 40 mm in length and at least 9 weeks old) have increased resistance to exposure to this disease (Blazer et al. 2003; Burckhardt and Hubert 2005; Ryce et al. 2005; Kerans et al. 2005; Krueger et al. 2006).


Means of Introduction: M. cerebralis was very likely introduced with nonindigenous salmonids that were stocked in the Great Lakes drainage system (Mills et al. 1993). It could have arrived with transfers of rainbow trout (Oncorhynchus mykiss) from Europe back to North America before 1956 (Crawford 2001).


Status: Established within the Great Lakes basin, although most occurrences have been at hatcheries and prevention and control measures have increased.


Great Lakes Impacts:  

Myxobolus cerebralis has a high environmental impact in the Great Lakes.
Realized:
Multiple salmonids are susceptible to infection by M. cerebralis, but the degree of susceptibility as well as symptom expression varies among species. Great Lakes native salmonid species susceptible to the pathogen include Atlantic Salmon (Salmo salar), Brook Trout (S. fontinalis), Cutthroat Trout (Oncorhynchus clarki), and Bull Trout (Salvelinus confluentus). In contrast, Lake Trout (S. namaycush) is not susceptible to infection (Bartholomew et al. 2003, Blazer et al. 2004, Gilbert and Granath 2003, Krueger et al. 2006, Sollid et al. 2003).

Historically, the realized environmental impacts of whirling disease on native Great Lakes aquacultured and wild species have been low (GLFHC 2006, GLFHC 2012). However, while M. cerebralis has not been detected in the Great Lakes region of Canada, the Canadian Food Inspection Agency (2012) lists it as a reportable disease. Such recognition warrants assessment of this species as having a high environmental effect for the region.

Potential:
In laboratory experiments, Myxobolus cerebralis myxospores infect the cosmopolitan oligochaete worm Tubifex tubifex (see Ecology) prior to development into a fish-infecting form (Elwell et al. 2009). Infection of T. tubifex can negatively affect the host’s growth, reproduction, and survival (DuBey et al. 2005, El-Matbouli and Hoffmann 1998, Gilbert and Granath 2003, Hedrick and El-Matbouli 2002, Stevens et al. 2001). However, such an impact on Great Lakes T. tubifex populations has not been reported.

While salmonid whirling disease has been problematic in hatcheries within the Great Lakes system, where stock can be seriously affected, M. cerebralis has also occurred in tributaries within the Great Lakes drainage system. Its persistence is likely being facilitated by infection of non-native salmonids present in this system (e.g., O. tshawytscha, O. kisutch, O. nerka, O. mykiss, Salmo trutta) (Mills et al. 1993, Ricciardi 2001).

Between 1987 and 2003, Gunnison River, Colorado, wild rainbow trout populations declined from approximately 11,000 to 86 fish within a 3.2 km stretch of water. This same trend was seen in at least five other Colorado rivers (Nehring 2006). In 1994, biologists discovered that whirling disease was the cause of declining wild rainbow trout populations in Colorado and Montana. What concerned biologists and managers most was an observed reduction in recruitment of 90 to 100 percent (Stromberg 2006). Myxobolus cerebralis also contributed to a decline in a native salmonid, the Yellowstone Cutthroat Trout (O. clarki bouvierii), in Yellowstone Lake, Wyoming (Koel et al. 2006). Impacts on Rainbow Trout have been documented in over 22 U.S. states and this disease has been reported in 25 U.S states (Elwell et al. 2009) and from 26 different countries (Gilbert and Granath 2003, Kallert et al. 2005). Though Cutthroat and Rainbow trout are not native to the Great Lakes, similar effects could be realized in Great Lakes native and salmonids as well as commercially valuable non-native (stocked) salmonids.

Whirling disease can alter fish community composition by replacing susceptible species with more resistant species such as Brown Trout (Elwell et al. 2009). This has been observed in several Montana drainages, where Rainbow Trout populations decreased while Brown Trout increased (Baldwin et al. 1998).

Whirling disease can result in whirling behavior or tail-chasing; damage to the central nervous system and organs of equilibrium; lesions in the skull, gills, and vertebrae; and sometimes mortality (Crawford 2001, Gilbert and Granath 2003, Krueger et al. 2006, Mills et al. 1993). This causes stress and leads to reduction in native fish populations by making it difficult for individuals to effectively escape predators or feed (WDI 2011). However, cascading food web effects as a result of M. cerebralis infection have not been reported in the Great Lakes.

There is little or no evidence to support Myxobolus cerebralis has a significant socio-economic impact in the Great Lakes.
Realized:
Whirling disease has no known human health effects (WDI 2006).

The multibillion dollar per year Great Lakes sport fishery and the multimillion dollar per year inland trout fishing industry are at risk if whirling disease becomes established in Wisconsin and Minnesota and/or continues to infect hatcheries and wild populations in Michigan (Frank 2002).

Potential:
The consequences of identifying this parasite in a hatchery can be severe, including facility closure, expensive renovations, and destruction of infected stock, leading to high economic costs. At a national level, trout fisheries—including the $325 million U.S. hatchery-raised rainbow trout industry (economic benefit reported 2004; USFWS 2006) that generated annual sales of more than $80 million from 2005-2007 (USDA 2008)—are especially at risk. In 2007, 86 percent of the United States’ 34.3 million trout intended for sale were lost due to a variety of diseases (USDA 2008). This percentage of state and federally raised hatchery trout intended for market but lost to disease rose to 90 percent in 2009 (USDA 2010). Furthermore, economic impacts realized at a regional level outside the Great Lakes as a result of M. cerebralis infection include a nearly 29 percent reduction in the total value of trout sales and the closure of six private hatcheries in Utah in 2005 (Stromberg 2006).

In 2006, low level infections of M. cerebralis spores were detected in Rainbow Trout reared in a Pennsylvania state hatchery. Whirling disease spores were also isolated from Pennsylvania’s Lake Erie steelhead in 1989, 1991, and 1997 (GLFHC 2006). However, wild trout populations of the mid-Atlantic region have not experienced observable declines, despite the presence of M. cerebralis and susceptible species (Hulbert 2005, Kaeser et al. 2006, Kaeser and Sharpe 2006).

In spring 2011, Michigan authorities conducted pre-stocking testing for M. cerebralis on nine representative lots of hatchery fish (60 fish per lot, including Brown Trout, Rainbow Trout, Chinook Salmon, Atlantic Salmon, Coho Salmon, Lake Trout, Brook Trout, Splake, and Lake Herring), and all were found negative for the parasite (GLFHC 2012). However, when conducting the same tests on wild-caught fish from hatchery water sources, molecular evidence of M. cerebralis was detected in one sample (containing pooled tissue of a total of 60 brown and rainbow trout from three sources— Slagle Creek, Harrietta Effluent Pond, and Brundage Spring Pond (GLFHC 2012).

There is little or no evidence to support that Myxobolus cerebralis has significant beneficial effects in the Great Lakes.


Management:  

Regulations (pertaining to the Great Lakes)
The Great Lakes Fish Disease Control Policy and Model Program have prohibited stocking the Great Lakes and their tributaries with fish from whirling disease infected farms. Fish imported into the North Central Region states must be certified free of whirling disease in order to obtain import permits (Faisal and Garling 2004).

Ohio requires out of state source facilities to document annual salmonid fish, egg, and sperm health inspections for one year prior to importation. Source facilities outside the Great Lakes basin must document health inspections for the previous five years with no whirling disease occurrences prior to importing salmonids into the Lake Erie watershed (Baird 2005). Indiana requires source facilities within the Great Lakes basin to document they have been whirling disease free for three consecutive years prior to importing salmonid stock. Source facilities outside the basin must document salmonid stocks have been whirling disease free consecutively since 2002 (Baird 2005). Michigan requires source facilities to document salmonid stocks have been whirling disease free for two consecutive years prior to importation, while Wisconsin requires one. Illinois and Minnesota also require imported salmonid health inspections. Minnesota allows the importation of whirling disease infected eggs, if prior egg treatments are approved (Baird 2005). Ontario requires an import permit issued by the Canadian Food Inspection Agency (CFIA) prior to the importation of certain finfish. Under the Canadian Health of Animals Act, aquaculturists are required to report any whirling disease suspicions to the CFIA (CFIA 2012).

All eight Great Lakes states (New York, Pennsylvania, Ohio, Michigan, Indiana, Illinois, Wisconsin, and Minnesota) have instated similar baitfish regulations to control the spread of whirling disease and other fish pathogens. Those of New York include that bait harvested from inland waters for personal use is only permitted to be used within the same body of water from which it was taken and cannot be transported overland (with the exception of smelt, suckers, alewives, and blueback herring). Once transported, baitfish cannot be replaced to its original body of water (NYSDEC 2012).

Live or frozen bait harvested from inland New York waters for commercial purposes is only permitted to be sold or possessed on the same body of water from which it was taken and cannot be transported over land unless under a permit and or accompanied by a fish health certification report. Bait that is preserved and packaged by any method other than freezing, such as salting, can be sold and used wherever the use of bait fish is legal as long as the package is labeled with the name of the packager-processor, the name of the fish species, the quantity of fish packaged, and the means of preservation (NYSDEC 2012).

Certified bait may be sold for retail and transported overland as long as the consumer maintains a copy of a sales receipt that contains the name of the selling vendor, date sold, species of fish sold, and quantity of fish sold. Bait that has not been certified may still be sold but the consumer must maintain a sales receipt containing the body of water where the bait fish was collected and a warning that the bait cannot be transported by motor vehicle. Bait sold for resale require a fish health certification along with a receipt that contains the name of the selling vendor, date sold, species of fish sold, and quantity of fish sold, which must be kept for 30 days or until all bait is sold (NYSDEC 2012).

In addition to baitfish protections, prior to placing fish in New York waters, a fish health certification report must document that the fish are whirling disease free.

Note: Check federal, state/provincial, and local regulations for the most up-to-date information.

Control
The following  biological, physical and chemical controls only pertain to fish in captive or hatchery operations. There are no known control methods of whirling disease in wild populations (except for management of spread - see Other below).

Biological
Managing T. tubifex populations can be implemented as a biocontrol of M. cerebralis. Maintaining water quality, reducing favorable habitat by preventing sediment accumulation in aquaculture (Crosier et al. 2012), and desiccating holding tanks, equipment, and intake pipes may help control T. tubifex (Kaster and Bushnell 1981). Lampricide TFM (3-triflouromethyl-4-nitrophenol), administered at (4.2-14.0 mg/L) doses, is effective at destroying T. tubifex (Liefers 1990). Tubifex tubifex can also be treated in 30°C water for four days, causing triactinomyxon (TAM) spore production to stop, thus preventing the next stage of the parasites life cycle (El-Matbouli et al. 1999).  Tubifex tubifex ability to support M. cerebralis’ triactinomyxon (TAM) spore production may be due to genetic differences among T. tubifex populations. This variability may be an important factor in determining infection rates among fish (Baxa et al. 2006) and therefore might support certain management practices (Stromberg 2006).
It has been proposed that selective processes are yielding a surviving population of fish that is more resistant to M. cerebralis infection on the Madison River, Montana (Vincent 2006). The implications of this for management are still unclear. However, research is continuing to evaluate the possibility of a developing resistance within salmonid populations(Stromberg 2006).

Physical
Managers have observed that using concrete in aquaculture facilities can reduce the abundance of T. tubifex and thus limit the ability of M. cerebralis to reproduce (Mills et al. 1993, Ricciardi 2001).

The Colorado Division of Wildlife (CDW 2011) administers routine fish health sampling at hatchery sites to help slow the spread of M. cerebralis infections by early detection. At the Roaring Judy Hatchery, a project is underway to install an ultraviolet system that kills M. cerebralis spores (CDW 2011).Treating water with 2537Å UV at doses of 35mWs/cm2 can be 86-100% effective at preventing whirling disease in rainbow trout fry (Hoffman 1974) and administering 1,300 mWs/cm2 of UV under a static collimated beam, can inactivate 100% of the TAM spores present (Hedrick et al. 2000).

There is evidence that electricity (1,000 s exposure to low-level DC voltage for 48 hrs) can destroy T. tubifex in aquaculture (R. Ingraham and T. Claxton, pers. comm. in Wagner 2002). Electrical charges of 1-3 kV pulsed 1-25 times at 99 µsec/pulse is effective at killing large numbers of TAM spores (Wagner 2002). Exposing myxospores to 90°C water for 10 minutes is also effective at destroying the spores (Hoffman and Markiw 1977).

Experiments by Hoffman (1974) have demonstrated that filtration is not an effective method for removing TAM spores from water – due to the small spores size, the filter needed to remove them slows flow to rates unacceptable for most applications.

Chemical
Hatchery intake water treated with chlorine (0.5 ppm) administered at two hour intervals once a week can reduce infection rates in rainbow trout by 63-73% without causing harm to the fish (Markiw 1992). Supply water treated with calcium cyanide (488 g/m2) mixed with chlorine gas (300 ppm) can be very effective at destroying M. cerebralis spores (Hoffman and Dunbar 1961). Water treated with chlorine (130-260 ppm) for 10 minutes may kill 100% of TAM spores present (Wagner 2002), and treating with chlorine (5,000 ppm) for 10 minutes is sufficient enough to destroy both triactinomyxon and myxospore (E. MacConnell, pers. comm. in Wagner 2002). Treating fry with chlorine (10 ppm) for 30 minutes may prevent whirling disease infection (Hoffman and O’Grodnick 1977).

It has been demonstrated that feeding rainbow trout with pellets containing (0.1%) Fumagillin is effective at reducing whirling disease infection. Two groups of Rainbow Trout were administered pellets from days 14-64 and 30-160 post infection. Approximately 10-20% of the medicated fish harbored spores, whereas 73-100% of non-medicated fish harbored spores (El-Matbouli and Hoffman 1991).

Earthen pond substrate treated with quicklime (CaO) at concentrations >380 g/m2 for two weeks prior to introducing fish can prevent whirling disease infection by destroying M. cerebralis spores (Hoffman and Hoffman 1972).

Other
Adherence to local laws regarding transportation of live fish between bodies of water, contacting local agencies immediately upon noticing signs of whirling disease, properly disposing of fish and fish parts, and not transporting mud on boots and shoes between bodies of water are useful in controlling the transmission of M. cerebralis spores in the wild.

Note: Check state/provincial and local regulations for the most up-to-date information regarding permits for control methods. Follow all label instructions.


Remarks: Taxonomically, Myxozoa is elevated to the highest level of classification (i.e. phylum), but this may formally become contained within the phylum Cnidaria within the next few years (R. Adlard, pers. comm. 2012).

Myxobolus cerebralis is synonymous with Myxosoma cerebralis.


References: (click for full references)

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Other Resources:
Author: Kipp, R.M., M. Cannister, and A.K. Bogdanoff.


Contributing Agencies:
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Revision Date: 8/16/2018


Citation for this information:
Kipp, R.M., M. Cannister, and A.K. Bogdanoff., 2018, Myxobolus cerebralis Hofer, 1903: U.S. Geological Survey, Nonindigenous Aquatic Species Database, Gainesville, FL, and NOAA Great Lakes Aquatic Nonindigenous Species Information System, Ann Arbor, MI, https://nas.er.usgs.gov/queries/GreatLakes/FactSheet.aspx?NoCache=2/28/2012+12:45:10+AM&SpeciesID=2364&State=&HUCNumber=4060200, Revision Date: 8/16/2018, Access Date: 11/19/2018

This information is preliminary or provisional and is subject to revision. It is being provided to meet the need for timely best science. The information has not received final approval by the U.S. Geological Survey (USGS) and is provided on the condition that neither the USGS nor the U.S. Government shall be held liable for any damages resulting from the authorized or unauthorized use of the information.