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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 [[chemosensitizer]]s, and trout mucous were ineffective (Wagner et al., 2002), as were anesthetized or dead fish (El-Matbouli et al., 1999). 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 (Vincent, 2002); using resistant species may help reduce the incidence and severity of whirling disease in aquaculture. There is also some circumstantial evidence that fish become resistant to the disease over time (Whirling Disease Foundation News, 2003). Additionally, [[aquaculture|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 (Markiw, 1992). Lastly, some drugs such as [[furazolidone]], [[furoxone]], [[benomyl]], [[fumagillin]], [[proguanil]] and [[clamoxyquin]] have been shown to impede spore development, which reduces infection rates (Markiw, 1992). For example, one study showed that feeding Fumagillin to ''[[
==Works Cited==
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