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Myxobolus cerebralis is an important myxozoan parasite of salmonids (salmon, trout, and allies) that causes whirling disease. It probably originated in Germany, but its range has expanded over the last hundred years to include most of Europe (including Russia), the United States, and South Africa (Bartholomew and Reno, 2002). It was originally thought that this parasite infected fish brains (hence the specific epithet cerebralis), however it quickly became apparent that it actually infects cartilage and skeletal tissue. Attempts to change the name to Myxobolus chondrophagus, which would more accurately describe the organism, failed because of nomenclature rules (Bartholomew and Reno, 2002). In the 1980’s, it was discovered that M. cerebralis also infects a tubificid oligochaete (a kind of segmented worm) between fishes (Markiw, 1992). Originally placed among the Protozoa, recent molecular studies suggest that myxozoans like M. cerebralis are in fact related to the Bilateria or Cnidaria, with Cnidaria being closer morphologically because both groups have extrusive filaments (Hedrick and El-Matbouli, 2002).
Morphology
M. cerebralis has many diverse stages ranging from single cells to relatively large spores, not all of which have been studied in detail. The stages that infect fish, called triactinomyxon spores, are made of a single style that is about 150 micrometers (μm) long and three processes or “tails” that are each about 200 micrometers long. A sporoplasm packet at the end of the style contains 64 germ cells surrounded by a cellular envelope (Hedrick and El-Matbouli, 2002). There are also three polar capsules, each of which contains a coiled polar filament between 170 and 180 μm long (Markiw, 1992). Polar filaments in both this stage and in the myxospore stage (see picture above) rapidly shoot into the body of the host, creating an opening through which the sporoplasm can enter. Triactinomyxons look so radically different from other Myxobolus stages that they were previously thought to be part of a separate class of organisms; organisms previously called Triactinomyxon dubium and T. gyrosalmo (class Actinosporea) are in fact triactinomyxon stages of M. cerebralis (Kent et al., 1994).
Myxospores, which develop from sporogonic cell stages inside fish hosts, are lenticular. They have a diameter of about 10 micrometers and are made of six cells. Two of these cells form polar capsules, two merge to form a binucleate sporoplasm, and two form protective valves (Hedrick and El-Matbouli, 2002). Myxospores are infective to oligochaetes, and are found among the remains of digested fish cartilage.
Life Cycle
Triactinomyxon spores swim through the water to infect a salmonid. Penetration of the fish by these spores takes only a few seconds. Within five minutes, a sporoplasm has entered the fish epidermis from within the spore, and within a few hours, the sporoplasm splits into individual germ cells that spread through the fish (Hedrick and El-Matbouli, 2002). Within the fish, there are both intracellular and extracellular stages that reproduce in its cartilage by endogeny, meaning that new cells grow from within old cells. The final stage within fish is the myxospore, which is formed by sporogony. They are released into the environment when the fish decomposes or is eaten (Hedrick and El-Matbouli, 2002). Some recent research indicates that some fish may expel viable myxospores while still alive (Nehring et al., 2002). The myxospore’s sporoplasm infects the worm by moving into the worm body after it is punctured by polar filaments (Hedrick and El-Matbouli, 2002). So far, the only worm known to be susceptible to M. cerebralis infection is Tubifex tubifex (Markiw, 1992). In the oligochaete, the binucleate sporoplasm of M. cerebralis lives in the intestinal wall and produces a variety of amoeboid cells by merogony, including pansporocysts. Pansporocysts include two generative cells that form gametocytes; the fusion of these gametocytes inside the pansporocyst forms a triactinomyxon spore that is released from the oligochaete anus into the water (Hedrick and El-Matbouli, 2002). Alternatively, a fish can become infected by eating an infected oligochaete (Markiw, 1992). Myxospores are extremely tough: “it was shown that Myxobolus cerebralis spores can tolerate freezing at 20° C for at least 3 months, aging in mud at 13° C for at least 5 months, and passage through the guts of northern pike Esox lucius or mallards Anas platyrhynchos without loss of infectivity” to worms (El-Matbouli and Hoffman, 1991). Triactinomyxons are much shorter lived, surviving 34 days or less, depending on temperature (Markiw, 1992a).
Pathology
M. cerebralis causes damage to its fish hosts through attachment of triactinomyxon spores and the migrations of various stages through tissues and along nerves, as well as by digesting cartilage (Hedrick and El-Matbouli, 2002). Aside from lesions on cartilage, internal organs generally appear healthy (Markiw, 1992). Other symptoms include skeletal deformities and “whirling” behavior (tail-chasing) in young fish, which is caused by “neural damage from lesions and disintegration of cartilaginous tissue around the organs of equilibrium,” and the tails of infected fish may also darken (Markiw, 1992).
Fish size, age, concentration of triactinomyxon spores, and water temperature all affect infection rates in fish, as does the species of the fish in question (Vincent, 2002). In one study of seven species of many strains, brook trout and rainbow trout (except one strain) were far more heavily affected by M. cerebralis after two hours of exposure than other species were, while bull trout, Chinook salmon, brown trout, and arctic grayling were least severely affected (Vincent, 2002). While brown trout may harbor the parasite, they do not show any symptoms, and this species may have been M. cerebralis' original host (Hoffman et al., 1962).
In T. tubifex, the release of triactinomyxon spores from the intestinal wall damages the worm’s mucosa; this may happen thousands of times in a single worm (Hedrick and El-Matbouli, 2002).
Impact
Where M. cerebralis has become well-established, it has caused decline or even elimination of whole generations of fish (Nehring, 1996; Vincent, 1996). The disease has the biggest impact on fish less than five months old because their skeleton has not ossified, and is susceptible to deforities (Halliday, 1975).
Prevention, Diagnosis and Treatment
Myxospores in fish are often difficult to distinguish from related species because of morphological similarities across genera. Though M. cerebralis is the only myxosporean ever found in salmonid cartilage, other visually similar species may be present in the skin, nervous system, or muscle (Markiw, 1992). The symptoms of whirling disease do not necessarily indicate its presence when taken individually in a single fish (“Injury or deficiency in dietary tryptophan and ascorbic acid can evoke similar signs”), but if a population shows all of them, then infection is likely (Markiw, 1992).
Some biologists have attempted to disarm triactinomyxon spores by making them fire prematurely. In the laboratory, only extreme acidity or basicity, moderate to high concentrations of salts, or electrical current caused premature filament discharge; neurochemicals, cnidarian chemosensitizers, and trout mucous were ineffective (Wagner et al., 2002), as were anesthetized or dead fish (El-Matbouli et al., 1999). If spores could be disarmed, they would be unable to infect fish, but it is unclear whether any of the methods that worked in the laboratory could be employed in the wild.
Some strains of fish are more resistant than others, even within species (Vincent, 2002); using resistant species may help reduce the incidence and severity of whirling disease in aquaculture. There is also some circumstantial evidence that fish become resistant to the disease over time (Whirling Disease Foundation News, 2003). Additionally, aquaculturists may avoid M. cerebralis infections by not using earthen ponds for raising young fish; this keeps them away from possibly infected tubificids and makes it easier to eliminate spores and oligochaetes through filtration, chlorination, and ultraviolet bombardment (Markiw, 1992). Lastly, some drugs such as furazolidone, furoxone, benomyl, fumagillin, proguanil and clamoxyquin have been shown to impede spore development, which reduces infection rates (Markiw, 1992). For example, one study showed that feeding Fumagillin to Oncorhynchus mykiss reduced the number of infected fish from between 73 and 100 percent to between 10 and 20 percent (El-Matbouli and Hoffman, 1991). Unfortunately, this treatment is considered unsuitable for wild trout populations (El-Matbouli & Hoffman, 1998).
Works Cited
- Bartholomew, J.L. and P.W. Reno. , 2002. The history and dissemination of whirling disease. American Fisheries Society Symposium 29:3-24.
- El-Matbouli, M., and R. W. Hoffmann., 1991. Effects of freezing, aging, and passage through the alimentary canal of predatory animals on the viability of Myxobolus cerebralis spores. Journal of Aquatic Animal Health 3(4):260-262.
- El-Matbouli, A. And R.w. Hoffmann. 1998. Light And Electron Microscopic Studies On The Chronological Development Of Myxobolus Cerebralis To The Actinosporean Stage In Tubifex Tubifes. International Journal For Parasitology 28:195-217.
- El-Matbouli, M., R. W. Hoffman, H. Shoel, T. S. McDowell, and R. P. Hedrick., 1999. Whirling disease: host specificity and interaction between the actinosporean stage of Myxobolus cerebralis and rainbow trout (Oncorhynchus mykiss) cartilage. Disease of Aquatic Organisms 35:1-12.
- Halliday, M.M. 1976. The Biology Of Myxosoma Cerebralis: The Causative Organism Of Whirling Disease Of Salmonids. Journal Of Fish Biology 9:339-357.
- Hedrick, R. P. and M. El-Matbouli. , 2002. Recent advances with taxonomy, life cycle, and development of Myxobolus cerebralis in the fish and oligochaete hosts. American Fisheries Society Symposium 29:45-53.
- Hoffman, G. 1962. Whirling Disease Of Trout. U.S. Department Of The Interior, Fishery Leaflet 508:1-3.
- Kent, M. L., L. Margolis, and J. O. Corliss., 1994. The demise of a class of protists: taxonomic and nomenclatural revisions proposed for the protist phylum Myxozoa Grasse, 1970. Canadian Journal of Zoology 72(5):932-937.
- Markiw, M. E., 1992. Salmonid whirling disease. Fish and Wildlife Leaflet 17.[1]
- Markiw, M. E., 1992a. Experimentally induced whirling disease. II. Determination of longevity of the infective triactinomyxon stage of Myxobolus cerebralis by vital staining. Journal of Aquatic Animal Health 4(1):44-47.
- Nehring, R.B. 1996. Whirling Disease In Feral Trout Populations In Colorado. In E.P. Bergersen And B.A.Knoph (eds.), Proceedings: Whirling Disease Workshop--where Do We Go From Here? Colorado Cooperative Fish And Wildlife Research Unit, Fort Collins. Pp. 126-144.
- Nehring, R. B. Thompson, K. G. Taurman, K. A. and D. L. Shuler. , 2002. Laboratory studies indicating that living brown trout Salmo trutta expel viable Myxobolus cerebralis myxospores. American Fisheries Society Symposium 29:125-134.
- Vincent, E.R. 1996. Whirling Disease--the Montana Experience, Madison River. In E.P. Bergersen And B.A.Knoph (eds.), Proceedings: Whirling Disease Workshop--where Do We Go From Here? Colorado Cooperative Fish And Wildlife Research Unit, Fort Collins. Pp. 159.
- Vincent, E. R. , 2002. Relative susceptibility of various salmonids to whirling disease with emphasis on rainbow and cutthroat trout. American Fisheries Society Symposium 29:109-115.
- Wagner, E. J. Cannon, Q. Smith, M. Hillyard, R. and R. Arndt. , 2002. Extrusion of Polar Filaments of the Myxobolus cerebralis Triactinomyxon by salts, electricity, and other agents. American Fisheries Society Symposium 29:61-76.
- Whirling Disease Foundation News. Jully, 2003. Research on whirling disease resistant rainbow trout. [2]