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.

[citation needed] Whirling disease affects juvenile fish (fingerlings and fry) and causes skeletal deformation and neurological damage.

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.

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

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.

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.

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.

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 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 behavior 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 less severe infections, the most common test involves digestion of the cranial cartilage with the proteases pepsin and trypsin (pepsin-trypsin digest—PTD) before looking for spores.

Parasite identity can also be confirmed using polymerase chain reaction to amplify the 415 base pair 18S rRNA gene from M. cerebralis.

Although originally a mild pathogen of Salmo trutta in central Europe and other salmonids in northeast Asia, the introduction 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, such as S. trutta, can become overloaded with parasites and incur 80%–90% mortalities.

The impact of M. cerebralis in Europe is somewhat lessened because the species is endemic to this region, giving native fish stocks a degree of immunity.

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.

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.

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 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.

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.

[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 vector Tubifex tubifex, the disease causing agent Myxobolus cerebralis, and/or related things out of the infected and buffer areas of Alberta.

In the laboratory, only extreme acidity or basicity, moderate to high concentrations of salts, or electric current caused premature filament discharge; neurochemicals, cnidarian chemosensitizers, and trout mucus were ineffective, as were anesthetized or dead fish.

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.

Lastly, some drugs, such as furazolidone, furoxone, benomyl, fumagillin, proguanil and clamoxyquine, have been shown to impede spore development, which reduces infection rates.