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Myxobolus cerebralis

2007 Schools Wikipedia Selection. Related subjects: Insects, Reptiles and
Fish

                           iMyxobolus cerebralis
   Triactinomyxon stage of Myxobolus cerebralis. Note the three "tails".
   Triactinomyxon stage of Myxobolus cerebralis. Note the three "tails".
                         Scientific classification

   Kingdom: Animalia
   Phylum:  Myxozoa
   Class:   Myxosporea
   Order:   Bivalvulida
   Family:  Myxobolidae
   Genus:   Myxobolus
   Species: M. cerebralis

                                Binomial name

   Myxobolus cerebralis
   Hofer, 1903

                                  Synonyms

   Myxosoma cerebralis
   Triactinomyxon dubium
   Triactinomyxon gyrosalmo

   Myxobolus cerebralis is a myxosporean parasite of salmonids ( salmon,
   trout, and their allies) that causes whirling disease in farmed salmon
   and trout and also in wild fish populations. It was first described
   from rainbow trout in Germany a century ago, but its range has spread
   and it has appeared in most of Europe (including Russia), the United
   States, South Africa^ and other countries. In the 1980s, it was
   discovered that M. cerebralis needs to infect a tubificid oligochaete
   (a kind of segmented worm) to complete its life-cycle.^ The parasite
   infects its hosts with its cells after piercing them with polar
   filaments ejected from nematocyst-like capsules.

   Whirling disease afflicts juvenile fish (fingerlings and fry) and
   causes skeletal deformation and neurological damage. Fish "whirl"
   rather than swim forward, find feeding difficult, and are more
   vulnerable to predators. The mortality rate is high for fingerlings, up
   to 90% of infected populations, and those that do survive are deformed
   by the parasite residing in their cartilage and bone. 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.

Taxonomy

   The taxonomy and naming of both M. cerebralis and of myxozoans in
   general have complicated histories. It was originally thought that this
   parasite infected fish brains (hence the specific epithet cerebralis),
   however it quickly became apparent that while it can be found in the
   nervous system, it primarily 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.^ Later, it became apparent that organisms previously called
   Triactinomyxon dubium and T. gyrosalmo ( class Actinosporea) were in
   fact triactinomyxon stages of M. cerebralis, whose life cycle was
   expanded to include the triactinomyxon stage.^ Similarly, other
   actinosporeans were folded into the life cycles of various
   myxosporeans.

   Today, the myxozoans, previously thought to be multicellular protozoans
   are considered animals by many scientists, though their status has not
   officially changed. Recent molecular studies suggest that they are
   related to Bilateria or Cnidaria, with Cnidaria being closer
   morphologically because both groups have extrusive filaments,^ but with
   Bilateria being somewhat closer in some genetic studies.^

Morphology

   Diagram of the structure of a triactionmyxon stage spore of Myxobolus
   cerebralis
   Enlarge
   Diagram of the structure of a triactionmyxon stage spore of Myxobolus
   cerebralis

   M. cerebralis has many diverse stages ranging from single cells to
   relatively large spores, not all of which have been studied in detail.

Triactinomyxon stage

   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.^ There are also three polar
   capsules, each of which contains a coiled polar filament between 170
   and 180 µm long.^ 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.

Sporoplasm stage

   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
   undergoes mitosis to produce more amoeboid cells, which migrate into
   deeper tissue layers, in order to reach the cerebral cartilage.^

Myxosporean stage

   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
   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.^

Life cycle

   Life cycle of M. cerebralis. Click to enlarge.
   Enlarge
   Life cycle of M. cerebralis. Click to enlarge.

   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 to M. cerebralis infection is Tubifex tubifex,^ though what
   scientists currently call T. tubifex may in fact be more than one
   species.^ First, myxospores are ingested by tubificid worms. In the gut
   lumen of the worm, the spores extrude their polar capsules and attach
   to the gut epithelium by polar 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 many amoeboid cells by an asexual cell fission process called
   merogony. 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 post-infection, sexual cell stages of the parasite
   undergo sporogenesis, and develop into pansporocysts, 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 1 year.^ The triactinomyxon
   spores swim through the water to 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 a sporoplasm has
   entered the fish epidermis, and within a few hours, the sporoplasm
   splits into individual cells that will spread through the fish.^

   Within the fish, there are both intracellular and extracellular stages
   that reproduce in its cartilage by asexual 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.^ Some recent research
   indicates that some fish may expel viable myxospores while still
   alive.^

   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.^ Triactinomyxons are much shorter lived,
   surviving 34 days or less, depending on temperature.^

Pathology

   Skeletal deformation in a mature Brook trout caused by M. cerebralis
   infection. Photo by Dr. Thomas L. Wellborn, Jr.
   Enlarge
   Skeletal deformation in a mature Brook trout caused by M. cerebralis
   infection. Photo by Dr. Thomas L. Wellborn, Jr.

   M. cerebralis infections have been reported from a wide range of
   salmonid species: 8 species of "Atlantic" salmonids, Salmo; 4 species
   of "Pacific" salmonids, Onchorhynchus; 4 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" behaviour (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 kill Myxobolus in their skin
   (possibly using antibodies), 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.^

   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, and it is believed that this can impair nutrient
   absorption.^ Also, infected worms have lower body mass and may be
   discolored.^ 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.^

Susceptibility

   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 biggest impact on fish less
   than five months old because their skeleton has not ossified. This
   makes young fish more susceptible to deformities^ and provides M.
   cerebralis more cartilage on which to feed.^ 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.^ While
   brown trout may harbour the parasite, they typically do not show any
   symptoms, and this species may have been M. cerebralis' original host.^
   This lack of symptoms in brown trout meant that the parasite was not
   discovered until after nonnative rainbow trout were introduced in
   Europe.^ The susceptibility of various salmonids is listed in Salmonid
   susceptibility to whirling disease.

Diagnosis

   The normally uniform trout cartilage is scarred with lesions in which
   M. cerebralis spores develop, weakening and deforming the connective
   tissues.
   Enlarge
   The normally uniform trout cartilage is scarred with lesions in which
   M. 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 behaviour and
   appearance about 35 to 80 days after initial infection, though "injury
   or deficiency in dietary tryptophan and ascorbic acid can evoke similar
   signs," so conclusive diagnosis may require finding myxospores in the
   fish's cartilage.^ In heavy infections, examining cartilage
   microscopically may be all that is needed to find spores.^ In less
   severe infections the most common test involves digestion of the
   cranial cartilage with the proteases pepsin and trypsin (the
   pepsin-trypsin digest—PTD) before looking for spores. The head and
   other tissues can be further examined using histopathology to confirm
   that the location and morphology of the spores matches what is known
   for M. cerebralis. Serological identification of spores in tissue
   sections using an antibody raised against the spores is also possible.
   Parasite identity can also be confirmed using the polymerase chain
   reaction to amplify the 415 base pair 18S rRNA gene from M.
   cerebralis.^Fish should be screened at the life stage most susceptible
   to the parasite. Routine screening using these techniques is carried
   out in countries where the parasite occurs and in countries like
   Australia and Canada that are not known to have the parasite but where
   its introduction could threaten local fish.

Impact

   M. cerebralis has been reported in Germany (1893), Italy (1954), USSR
   (1955), including Sakhalin Island (1960), USA (1958), Bulgaria (1960),
   Yugoslavia (1960), Sweden (1966), South Africa (1966), Scotland (1968),
   New Zealand (1971), Ecuador (1971), Norway (1971), Colombia (1972),
   Lebanon (1973), Ireland (1974), Spain (1981) and England (1981)
   Enlarge
   M. cerebralis has been reported in Germany (1893), Italy (1954), USSR
   (1955), including Sakhalin Island (1960), USA (1958), Bulgaria (1960),
   Yugoslavia (1960), Sweden (1966), South Africa (1966), Scotland (1968),
   New Zealand (1971), Ecuador (1971), Norway (1971), Colombia (1972),
   Lebanon (1973), Ireland (1974), Spain (1981) and England (1981)

   Although originally a mild pathogen of Salmo trutta in central Europe
   and other salmonids in north east Asia, the spread of the Rainbow trout
   (Oncorhynchus mykiss) has greatly increased the impact of this
   parasite. Having no innate immunity to M. cerebralis, rainbow trout are
   particularly susceptible, and can release so many spores that even more
   resistant species in the same area, like S. trutta, can become
   overloaded with parasites and incur 80%–90% mortalities. Where M.
   cerebralis has become well-established, it has caused decline or even
   elimination of whole cohorts of fish.^ ^

Impact in Europe

   The impact of M. cerebralis in Europe is somewhat lessened by the fact
   that the species is endemic to this region, giving native fish stocks a
   degree of immunity. Rainbow trout, the most susceptible species to this
   parasite, are not native to Europe; successfully reproducing feral
   populations are rare, so there are few wild rainbow trout that are
   young enough to be susceptible to infection. On the other hand, they
   are widely reared for restocking sport-fishing waters and for
   aquaculture, 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 in order to guard against spore introduction during water
   exchanges.^ Fry are moved to earthen ponds only when they are
   considered to be clinically resistant to the parasite, after skeletal
   ossification occurs.^

Impact in New Zealand

   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 is quarantine restriction placed on exports of salmon products
   to Australia.

Impact in the United States

   M. cerebralis has been reported in nearly two dozen (green) states in
   the United States, according to the Whirling Disease Initiative
   Enlarge
   M. cerebralis has been reported in nearly two dozen (green) states in
   the United States, according to the Whirling Disease Initiative

   M. cerebralis was first recorded in North America in 1956 in
   Pennsylvania, 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, "the Montana Whirling Disease Task Force estimated that trout
   fishing generated US $300,000,000 in recreational expenditures in
   Montana alone".^ Making matters worse, some of the fishes that M.
   cerebralis infects ( bull trout, cutthroat trout, and steelhead) are
   already threatened or endangered, 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 in
   California, Michigan, and New York.^

Prevention and control

   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,^ as were
   anesthetized or dead fish.^ 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^ ; 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 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.^ To minimise tubificid
   population 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 as furazolidone, furoxone, benomyl, fumagillin,
   proguanil and clamoxyquine have been shown to impede spore development,
   which reduces infection rates.^ For example, one study showed that
   feeding Fumagillin to Oncorhynchus 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 States Food and Drug Administration
   approval.^

   Recreational and sports fishers can help to prevent the spread of the
   parasite in a number of ways. Cleaning fishing equipment between
   fishing trips and never transporting fish from one body of water to
   another should protect against cross contamination of waterways. Spores
   are particularly persistent in felt soled wading shoes, which can be
   treated with 10% chlorine bleach and water for at least 15 minutes and
   then rinsed thoroughly. Fish bones or entrails should never be disposed
   of in any body of water, since spores from the carcass will be released
   into the waterway. Salmon and trout should not be used as bait.
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