El-Matbouli et al. (1999) note that the spores of M. cerebralis demonstrate classic characteristics of the Myxozoa phylum. They have thin polar filaments (50 nm in diameter), which can be everted from the polar capsule in response to stimuli. Spore appearance differs depending on the host.

According to Kent et al. (2001), Myxobolus cerebralis has a two-host life cycle that involves the fish and an alternate host, the bottom-dwelling tubifex worm (Tubifex tubifex). When an infected fish dies and decays, spores are released and ingested by tubifex worms. The spores undergo development in the worm's intestine and multiply rapidly. When released by the worm, the water-borne spores infect susceptible fish by attaching to the fish's body. The parasite then migrates through the skin to the central nervous system, and ultimately into the cartilage of the fish. The spores are believed to be capable of remaining dormant in mud for thirty years (Storey, 2003).

Melrose (2002) states that oligochaete worms and all species of trout and salmon may be susceptible to the M. cerebralis parasite. Rainbow trout and cutthroat trout appear to be more susceptible than other trout species.

Melrose (2002) characterises Myxobolus cerebralis reproduction in three distinct processes. First, sporogony occurs immediately after a sexual phase and consists of an asexual reproduction that culminates in the production of sporozoites. Secondly, sporozoites will develop into forms that undergo another asexual replication known as merogony. In some species merogony is also referred to as schizogony. Finally, and as an alternative to asexual replication, schizogonites can become gametes through a process variously called gametogamy or gametogony.

According to Kent et al. (2001), Myxobolus cerebralis is a metazoan parasite that penetrates the head and spinal cartilage of fingerling trout where it multiplies very rapidly, putting pressure on the organ of equilibrium. This causes the fish to swim erratically (hence the name, whirling disease) and have difficulty feeding and avoiding predators. This disease has pronounced economic effects. It is responsible for high mortalities in hatchery fry and fingerling salmonids, especially rainbow trout. As finfish aquaculture has increased dramatically in the United States since the 1990's, the problem has been the focus of a growing amount of research. As the disease has now been detected in some wild populations, it may also decrease revenue from recreational fisheries.

Preventative measures: According to Melrose (2002), no known treatments exist to counteract the effects of M. cerebralis in infected organisms. Those fish that do recover still retain the physical damage associated with infection. To decrease or prevent economic losses, various management techniques have and are being developed for use in fish hatcheries. As young fish are the most susceptible, management techniques have traditionally focused on controlling exposure of fry to the infectious stage of M. cerebralis, which are microscopic spores called triactinomyxons. Hatcheries have previously done this in two ways: 1) rear the young fish in well water to prevent exposure until they are older and more resistant, or 2) use pond designs that reduce potential habitat for oligochaetes. New research suggests that exposing water to unltraviolet light can inactivate triactinomyxons. A dose of 1300 mWs cm-2 ultraviolet light can inactivate 100% of the triactinomyxon sporoplasm cells. Sporoplasm is the infective mass of protoplasm within the spore that is injected into the host cell by various parasitic microorganisms.

The Whirling Disease Foundation, the Whirling Disease Initiative, and sponsored researchers are leading research on the development of a working risk assessment model for whirling disease and how it might be used as a management tool by fisheries managers to estimate risks and identify actions to reduce these risks. For details and updates on this project please see Whirling Disease Initiative: Risk Assessment.