Whirling Disease (Myxosoma cerebralis)
Symptoms:
Clinically fish become deformed about the head and spine with the fish swimming erratically (whirling). Histologically there is necrosis of the cartilage with numerous spores present in the area of inflammation. The necrosis of the cartilage is the cause of the deformation.
Causes:
Myxosporidean parasite with a 10 micron oval spore with 2 piriform polar capsules. Parasite affects primarily young salmonids (rainbow trout most susceptible).
Transmission is believed to be by ingestion of spores. The life cycle of this organism is not completely known (believed to be indirect since myxobolus spores do not directly infect the fish) however, there appears to be a tubeficid oligochaetes (tubifex mud worm) as an important intermediate or transport host. It is believed that the parasite undergoes sporulation in the tubiflex worm were the organism takes on the form of a Triactinomyxon sp. It is believed that this parasite is then released from the tubifex worm and infects the trout. (ingestion of infected tubifex worms may also cause the fish to become infected)
Morphology
All information retrieved from Wikipedia for reference and archival purposes.
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
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.
Treatment:
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.
