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| Myxobolus cerebralis | |
|---|---|
 | |
| Triactinomyxon stage ofMyxobolus cerebralis - note the three "tails" | |
Scientific classification | |
| Domain: | Eukaryota |
| Kingdom: | Animalia |
| Phylum: | Cnidaria |
| Class: | Myxosporea |
| Order: | Bivalvulida |
| Family: | Myxobolidae |
| Genus: | Myxobolus |
| Species: | M. cerebralis |
| Binomial name | |
| Myxobolus cerebralis Hofer, 1903 | |
| Synonyms | |
Myxosoma cerebralis | |
Myxobolus cerebralis is amyxosporeanparasite ofsalmonids (salmon andtrout species) that causes whirling disease infarmed salmon and trout and also inwild fish populations. It was first described inrainbow trout in Germany in 1893, but its range has spread and it has appeared in most of Europe (including Russia), the United States, South Africa, Canada and other countries from shipments of cultured and wild fish. In the 1980s,M. cerebralis was found to require atubificidoligochaete (a kind ofsegmented worm) to complete its life cycle. The parasite infects its hosts with its cells after piercing them withpolar filaments ejected fromnematocyst-like capsules. This infects the cartilage and possibly the nervous tissue of salmonids, causing a potentially lethal infection in which the host develops a black tail, spinal deformities, and possibly more deformities in the anterior part of the fish.[citation needed]
Whirling disease affectsjuvenile fish (fingerlings and fry) and causesskeletal deformation andneurological damage. Fish "whirl" forward in an awkward, corkscrew-like pattern instead of swimming normally, find feeding difficult, and are more vulnerable to predation. The mortality rate is high for fingerlings, up to 90% of infected populations, and those that do survive are deformed by the parasites residing in theircartilage,bone, and neurological tissue. They act as a reservoir for the parasite, which is released into water following the fish's death.M. cerebralis is one of the most economically important myxozoans in fish, as well as one of the most pathogenic. It was the first myxosporean whose pathology and symptoms were described scientifically. The parasite is not transmissible to humans.
Thetaxonomy and naming of bothM. cerebralis, and ofmyxozoans in general, have complicated histories. It was originally thought to infect fish brains (hence thespecific epithetcerebralis) andnervous systems, though it soon was found to primarily infectcartilage,skeletal tissue, and nervous tissue. Attempts to change the name toMyxobolus chondrophagus, which would more accurately describe the organism, failed because ofnomenclature rules[which?].[citation needed] Later, the organisms previously calledTriactinomyxon dubium andT. gyrosalmo (classActinosporea) were found to be, in fact,triactinomyxon stages ofM. cerebralis, the life cycle of which was expanded to include the triactinomyxon stage. Similarly, other actinosporeans were folded into the life cycles of various myxosporeans.[citation needed]
M. cerebralis is one of the 1,350 known myxozoan parasites known to infect fish.[1] Once thought to be a species ofProtozoa, taxonomists noticed characteristics that more closely relatedM. cerebralis to the phylumCnidaria. These features included cnidocysts, which are tentacles that are used to hold onto and prey upon the host.M. cerebralis has many diverse stages ranging from singlecells to relatively large spores, not all of which have been studied in detail. This complex lifecycle involves two different hosts and numerous developmental stages. These stages happen through mitosis, endogeny, plasmotomy, or possibly meiosis. In the first part of its lifecycle,M. cerebralis is attached to its salmonid host externally. They then use their stinging tentacles to infect the host, causing the skeletal tissues and nervous system to become deformed.
Today, the myxozoans, previously thought to be multicellular protozoans, are consideredanimals by most scientists, though their status has not officially changed. Recent molecular studies suggest they are related toBilateria orCnidaria, with Cnidaria being closer morphologically because both groups have extrusive filaments. Bilateria were somewhat closer in some genetic studies, but those were found to have used samples that were contaminated by material from the host organism, and a 2015 study confirms they are cnidarians.[citation needed]
M. cerebralis has many diverse stages ranging from singlecells to relatively large spores, not all of which have been studied in detail.
The stages that infect fish, calledtriactinomyxon spores, are made of a single style that is about 150micrometers (μm) long and three processes or "tails", each about 200 micrometers long. These spores are typically oval shaped, and display asymmetrical symmetry. Asporoplasm packet at the end of the style contains 64 germ cells surrounded by a cellular envelope. There are also threepolar capsules, each of which contains a coiledpolar filament between 170 and 180 μm long, with about 5-6 coils in each filament. Polar filaments in both this stage and in themyxospore stage (see picture above) rapidly shoot into the body of the host, creating an opening through which the sporoplasm can enter. When it develops this polar filament it is able to attach to its host.
Upon contact with fish hosts and firing of the polar capsules, the sporoplasm contained within the central style of the triactinomyxon migrates into the epithelium or gut lining. Firstly, this sporoplasm undergoesmitosis to produce moreamoeboid cells, which migrate into deeper tissue layers, to reach the cerebral cartilage.
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. Myxospores are infective to oligochaetes, and are found among the remains of digested fish cartilage. They are often difficult to distinguish from related species because of morphological similarities acrossgenera. ThoughM. cerebralis is the only myxosporean ever found in salmonid cartilage, other visually similar species may be present in the skin,nervous system, ormuscle.
Myxobolus cerebralis has a two-host life cycle involving a salmonid fish and a tubificid oligochaete. So far, the only worm known to be susceptible toM. cerebralis infection isTubifex tubifex, though what scientists currently callT. tubifex may in fact be more than one species. First, myxospores are ingested by tubificid worms. In thegutlumen of the worm, the spores extrude theirpolar capsules and attach to the gutepithelium bypolar filaments. The shell valves then open along the suture line and the binucleate germ cell penetrates between the intestinal epithelial cells of the worm. This cell multiplies, producing manyamoeboid cells by an asexual cellfission process calledmerogony. As a result of the multiplication process, the intercellular space of the epithelial cells in more than 10 neighbouring worm segments may become infected.
Around 60–90 days postinfection, sexual cell stages of the parasite undergosporogenesis, and develop intopansporocysts, each of which contains eight triactinomyxon-stage spores. These spores are released from the oligochaete anus into the water. Alternatively, a fish can become infected by eating an infected oligochaete. Infected tubificids can release triactinomyxons for at least a year. The triactinomyxon spores are carried by the water currents, where they can infect a salmonid through the skin. Penetration of the fish by these spores takes only a few seconds. Within five minutes, a sac of germ cells called asporoplasm has entered the fishepidermis, and within a few hours, the sporoplasm splits into individual cells that will spread through the fish.
Within the fish, both intracellular and extracellular stages reproduce in its cartilage by asexualendogeny, meaning new cells grow from within old cells. The final stage within the fish is the creation of the myxospore, which is formed bysporogony. They are released into the environment when the fish decomposes or is eaten. Some recent research indicates some fish may expel viable myxospores while still alive.
Myxospores are extremely tough: "it was shown thatMyxobolus 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 ofnorthern pikeEsox lucius ormallardsAnas platyrhynchos without loss of infectivity" to worms.[citation needed] Triactinomyxons are much shorter-lived, surviving 34 days or less, depending on temperature.[citation needed]
M. cerebralis infections have been reported from a wide range of salmonid species: eight species of "Atlantic" salmonids,Salmo; four species of "Pacific" salmonids,Oncorhynchus; four species of char,Salvelinus; the grayling,Thymallus thymallus; and the huchen,Hucho hucho.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. The fish's tail may darken, but aside from lesions on cartilage, internal organs generally appear healthy. Other symptoms include skeletal deformities and "whirling" behavior (tail-chasing) in young fish, which was thought to have been caused by a loss of equilibrium, but is actually caused by damage to the spinal cord and lower brain stem. Experiments have shown that fish can killMyxobolus in their skin (possibly usingantibodies), but that the fish do not attack the parasites once they have migrated to the central nervous system. This response varies from species to species.
InT. tubifex, the release of triactinomyxon spores from theintestinal wall damages the worm'smucosa; this may happen thousands of times in a single worm, and is believed to impair nutrient absorption. Spores are released from the worm almost exclusively when the temperature is between 10 °C and 15 °C, so fish in warmer or cooler waters are less likely to be infected, and infection rates vary seasonally.
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. The disease has the most impact on fish less than five months old because their skeletons have notossified. This makes young fish more susceptible to deformities and providesM. cerebralis more cartilage on which to feed. In one study of seven species of many strains,brook trout andrainbow trout (except one strain) were far more heavily affected byM. cerebralis after two hours of exposure than other species were, whilebull trout,Chinook salmon,brown trout, andArctic grayling were least severely affected. While brown trout may harbor the parasite, they typically do not show any symptoms, and this species may have beenM. cerebralis' original host. This lack of symptoms in brown trout meant that the parasite was only discovered after nonnative rainbow trouts were introduced in Europe.
The normally uniform trout cartilage is scarred with lesions in whichM. cerebralis spores develop, weakening and deforming the connective tissues.
Moderate or heavy clinical infection of fish with whirling disease can be presumptively diagnosed on the basis of changes in behavior and appearance about 35 to 80 days after initial infection, though "injury or deficiency in dietarytryptophan andascorbic acid can evoke similar signs", so conclusive diagnosis may require finding myxospores in the fish's cartilage. In heavy infections, only examining cartilage microscopically may be necessary to find spores. In less severe infections, the most common test involves digestion of the cranial cartilage with theproteasespepsin andtrypsin (pepsin-trypsin digest—PTD) before looking for spores. The head and other tissues can be further examined usinghistopathology to confirm whether the location and morphology of the spores matches what is known forM. cerebralis. Serological identification of spores in tissue sections using anantibody raised against the spores is also possible. Parasite identity can also be confirmed usingpolymerase chain reaction to amplify the 415 base pair18S rRNAgene fromM. cerebralis. Fish should be screened at the life stage most susceptible to the parasites, with particular focus on fish in aquaculture units.
Although originally a mild pathogen ofSalmo trutta in central Europe and other salmonids in northeast Asia, the introduction of therainbow trout (Oncorhynchus mykiss) has greatly increased the impact of this parasite. Having no innate immunity toM. cerebralis, rainbow trout are particularly susceptible, and can release so many spores that even more resistant species in the same area, such asS. trutta, can become overloaded with parasites and incur 80%–90% mortalities. WhereM. cerebralis has become well-established, it has caused decline or even elimination of whole cohorts of fish.
The impact ofM. cerebralis in Europe is somewhat lessened because the species is endemic to this region, giving nativefish stocks a degree ofimmunity. Rainbow trout, the most susceptible species to this parasite, are not native to Europe; successfully reproducingferal populations are rare, so few wild rainbow trout are young enough to be susceptible to infection. On the other hand, they are widely reared for restockingsport-fishing waters and foraquaculture, where this parasite has its greatest impact. Hatching and rearing methods designed to prevent infection of rainbow trout fry have proved successful in Europe. These techniques include hatching eggs in spore-free water and rearing fry to the "ossification" stage in tanks or raceways. These methods give particular attention to the quality of water sources to guard against spore introduction during water exchanges. Fry are moved to earthen ponds only once they are considered to be clinically resistant to the parasite, after skeletal ossification occurs. However, some Norwegian facilities have gotten outbreaks ofM. cerebralis causing millions of dollars in loss.
M. cerebralis was first found in New Zealand in 1971. The parasite has only been found in rivers in the South Island, away from the most important aquaculture sites. Additionally, salmonid species commercially aquacultured in New Zealand have low susceptibility to whirling disease, and the parasite has also not been shown to affect native salmonids. An important indirect effect of the parasites presence isquarantine restriction placed onexports of salmon products to Australia.
M. cerebralis has been reported in nearly two dozen (green) states in the United States, according to the Whirling Disease InitiativeM. cerebralis was first recorded in North America in 1956 inPennsylvania, having been introduced via infected trout imported from Europe, and has spread steadily south and westwards. Until the 1990s, whirling disease was considered a manageable problem affecting rainbow trout in hatcheries. However, it has recently become established in natural waters of the Rocky Mountain states (Colorado,Wyoming,Utah,Montana,Idaho,New Mexico), where it is causing heavy mortalities in several sportfishing rivers. Some streams in the western United States have lost 90% of their trout. In addition, whirling disease threatens recreational fishing, which is important for the tourism industry, a key component of the economies of some U.S. western states. For example, "theMontana Whirling Disease Task Force estimated trout fishing generated US $300,000,000 in recreational expenditures in Montana alone". Making matters worse, some of the fish species thatM. cerebralis infects (bull trout,cutthroat trout, andsteelhead) are already threatened orendangered, and the parasite could worsen their already precarious situations. For reasons that are poorly understood, but probably have to do with environmental conditions, the impact on infected fish has been greatest in Colorado and Montana, and least inCalifornia,Michigan, and New York.
Whirling disease was first confirmed in fish inJohnson Lake inBanff National Park in August, 2016.[2]CFIA Labs confirmed in August andParks Canada announced the outbreak August 23, 2016. Although it was first discovered in Banff, it is not necessarily where the disease originated and spread. The Government of Alberta is currently sampling and testing fish in 6 different watersheds (Peace River, Athabasca, North Saskatchewan, Red Deer, Bow and Oldman) to see where the disease has spread. Initial sample fish were collected in 2016, and are currently being processed by the Government of Alberta and CFIA labs. Since testing began, it has been detected in the Upper Bow River, and in May 2017 it was confirmed that whirling disease had also been detected in the Oldman River Basin. The declaration does not mean that every susceptible finfish population within the Bow and Oldman River watersheds are infected with the disease.[citation needed]
The parasite was first detected in the adjacent province ofBritish Columbia in January, 2024.[3]
As a result of the new declaration, a domestic movement permit will be required from the CFIA for susceptible species and end uses identified in the Domestic Movement Control Program, the vectorTubifex tubifex, the disease causing agentMyxobolus cerebralis, and/or related things out of the infected and buffer areas of Alberta. Recreational and sport fishing, including fishing led by a professional guide, will not require a CFIA permit.
Some biologists have attempted to disarm triactinomyxon spores by making them fire prematurely. In the laboratory, only extremeacidity orbasicity, moderate to high concentrations of salts, or electric current caused premature filament discharge; neurochemicals, cnidarianchemosensitizers, and trout mucus were ineffective, as were anesthetized or dead fish. If spores could be disarmed, they would be unable to infect fish, but further research is needed to find an effective treatment.
Some strains of fish are more resistant than others, even within species; using resistant strains may help reduce the incidence and severity of whirling disease in aquaculture. There is also some circumstantial evidence that fish populations can develop resistance to the disease over time. Additionally, aquaculturists may avoidM. 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. To minimise tubificid populations, techniques include periodic disinfection of the hatchery or aquaculture ponds, and the rearing of small trout indoors in pathogen-free water. Smooth-faced concrete or plastic-lined raceways that are kept clean and free of contaminated water keep aquaculture facilities free of the disease.
Lastly, some drugs, such asfurazolidone,furoxone,benomyl,fumagillin,proguanil andclamoxyquine, have been shown to impede spore development, which reduces infection rates. For example, one study showed that feeding fumagillin toO. mykiss reduced the number of infected fish from between 73% and 100% to between 10% and 20%. Unfortunately, this treatment is considered unsuitable for wild trout populations, and no drug treatment has ever been shown to be effective in the studies required for United StatesFood and Drug Administration approval.
Recreational and sports fishers can help to prevent the spread of the parasite by not transporting fish from one body of water to another, not disposing of fishbones or entrails in any body of water, and ensuring boots and shoes are clean before moving between different bodies of water. Federal, state, provincial, and local regulations on the use ofbait should be followed.
