Шабақ ауруы: Myxobolus cerebralis паразитінің сипаттамасы

Species of parasite

Myxobolus cerebralis is a myxosporean parasite of salmonids (salmon and trout species) that causes whirling disease in farmed salmon and trout and also in wild fish populations. It was first described in rainbow 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 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. 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. Whirling disease affects juvenile fish (fingerlings and fry) and causes skeletal deformation and neurological 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 their cartilage, 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. The taxonomy and naming of both M. cerebralis, and of myxozoans in general, have complicated histories. It was originally thought to infect fish brains (hence the specific epithet cerebralis) and nervous systems, though it soon was found to primarily infect cartilage, skeletal tissue, and nervous tissue. Attempts to change the name to Myxobolus chondrophagus, which would more accurately describe the organism, failed because of nomenclature rules. Later, the organisms previously called Triactinomyxon dubium and T. gyrosalmo (class Actinosporea) were found to be, in fact, triactinomyxon stages of M. 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.

M. cerebralis is one of the 1,350 known myxozoan parasites known to infect fish. Once thought to be a species of Protozoa, taxonomists noticed characteristics that more closely related M. cerebralis to the phylum Cnidaria. 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 single cells 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 considered animals by most scientists, though their status has not officially changed. Recent molecular studies suggest they are related to Bilateria or Cnidaria, 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.

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", each about 200 micrometers long. These spores are typically oval shaped, and display asymmetrical symmetry. 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, with about 5 6 coils in each filament. 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. 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 undergoes mitosis to produce more amoeboid 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 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.

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 postinfection, 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 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 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, both intracellular and extracellular stages reproduce in its cartilage by asexual endogeny, meaning new cells grow from within old cells. The final stage within the fish is the creation of the myxospore, which is formed by sporogony. 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 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.

Skeletal deformation in a mature brook trout caused by M. cerebralis infection. 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 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 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.