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Montrose, CO, United States

Barry Nehring R.,300 South Townsend Avenue | Hancock B.,Colorado State University | Catanese M.,Colorado State University | Stinson M.E.T.,Colorado State University | And 3 more authors.
Journal of Aquatic Animal Health | Year: 2013

Elucidating the dynamics of a parasitic infection requiring two hosts in a natural ecosystem can be a daunting task. Myxobolus cerebralis (Mc), the myxozoan parasite that causes whirling disease in some salmonids, was detected in the Colorado River upstream of Windy Gap Reservoir (WGR) in 1988. Subsequently, whirling disease was implicated in the decline of wild Rainbow Trout Oncorhynchus mykiss in the river when WGR was identified as a point source of Mc triactinomyxons (TAMs). Between 1997 and 2004, numerous investigations began to elucidate the etiology of Mc in WGR. During this period, Mc TAM production in WGR declined more than 90%. Explanations for the decline have included differences in stream discharge between years, changes in the thermal regime of the lake, severe drought, changes in the fish population structure in WGR, and reductions in the prevalence and severity of Mc infection in salmonids in the Colorado and Fraser rivers upstream of WGR. All of these have been discredited as explanations for the reduced TAM production. In 2005, a new study was conducted to replicate the studies completed in 1998. In this paper, the results of a new real-time polymerase chain reaction assay utilized to quantify the mitochondrial 16S rDNA specific to each of four lineages of Tubifex tubifex in pooled samples of 50 oligochaetes are presented. These results suggest that compared with 1998, the densities of aquatic oligochaetes and T. tubifex have increased, TAM production has been greatly reduced, and the decline is congruent with the dominance of lineages I, V, and VI of T. tubifex-three lineages that are refractory or highly resistant to Mc infection-in the oligochaete population. While it is possible that the resistant lineages function as biofilters that deactivate Mc myxospores, the reason for the decline in TAM production in WGR remains an enigma. © American Fisheries Society 2013. Source

Thompson K.G.,300 South Townsend Avenue
Aquatic Ecosystem Health and Management | Year: 2011

The effects on trout of the whirling disease parasite Myxobolus cerebralis were evaluated to observe whether they could be ameliorated by intervening with physical habitat manipulations. Physical stream habitat was modified at field sites in Spring Creek and Williams Fork River, Colorado, USA to reduce or eliminate habitat for the invertebrate oligochaete host of M. cerebralis, Tubifex tubifex. Datawere collected before and after habitat modifications on total oligochaete and T. tubifex biomass, actinospore production from oligochaete samples, surface water actinospore concentrations, and prevalence and intensity of myxospore development in Brown Trout, Salmo trutta. Oligochaete biomass estimates lacked precision due to inherently patchy distribution of the target organisms. Oligochaetes quickly re-occupied a portion of habitat at the Williams Fork River site, but oligochaete biomass was depressed for nearly a year at the Spring Creek site. All T. tubifex in Spring Creek belonged to a susceptible lineage, but in the Williams Fork River there was amix of susceptible and non-susceptible T. tubifex. Actinospore detection in filtered surface water samples showed consistent but minor reduction in density in Williams Fork River and no difference or even higher densities in Spring Creek after habitat modification. Myxospore prevalence and intensity of infection in Brown Trout appeared to decrease in Williams Fork River after habitat modification, but there is evidence that a similar decrease also occurred at a control site in that stream. Spring Creek showed no effect for these metrics. The differing responses may have been influenced by T. tubifex lineage differences. The habitat manipulations did not show sufficient promise to encourage further efforts in Colorado. © 2011 AEHMS. Source

Barry Nehring R.,300 South Townsend Avenue | Lukacs P.M.,University of Montana | Baxa D.V.,University of California at Davis | Stinson M.E.T.,300 South Townsend Avenue | And 4 more authors.
Journal of Aquatic Animal Health | Year: 2014

Establishment of Myxobolus cerebralis (Mc) resulted in declines of wild Rainbow Trout Oncorhynchus mykiss populations in streams across Colorado during the 1990s. However, the risk for establishment and spread of this parasite into high-elevation habitats occupied by native Cutthroat Trout O. clarkii was unknown. Beginning in 2003, tubificid worms were collected from all major drainages where Cutthroat Trout were endemic and were assayed by quantitative PCR to determine the occurrence and distribution of the various lineages of Tubifex tubifex (Tt) oligochaetes. Over a 5-year period, 40 groups of Tt oligochaetes collected from 27 streams, 3 natural lakes, 2 private ponds, and a reservoir were evaluated for their relative susceptibility to Mc. Exposure groups were drawn from populations of pure lineage III Tt, mixed-lineage populations where one or more of the highly resistant (lineage I) or nonsusceptible lineages (V or VI) were the dominant oligochaete and susceptible lineage III worms were the subdominant worm, or pure lineage VI Tt. Experimental replicates of 250 oligochaetes were exposed to 50 Mc myxospores per worm. The parasite amplification ratio (total triactinomyxons [TAMs] produced / total myxospore exposure) was very high among all pure lineage III Colorado exposure groups, averaging 363 compared with 8.24 among the mixed-lineage exposure groups. Lineage III oligochaetes from Mt.Whitney Hatchery in California, which served as the laboratory standard for comparative purposes, had an average parasite amplification ratio of 933 among 10 exposed replicates over a 5-year period. Lineage I oligochaetes were highly resistant to infection and did not produce any TAMs. Lineages V and VI Tt did not become infected and did not produce any TAMs. These results suggest that the risk of establishment of Mc is high for aquatic habitats in Colorado where Cutthroat Trout and lineage III Tt are sympatric. Source

Barry Nehring R.,300 South Townsend Avenue | Schisler G.,17 West Prospect Street | Chiaramonte L.,300 South Townsend Avenue | Horton A.,300 South Townsend Avenue | Poole B.,300 South Townsend Avenue
Journal of Aquatic Animal Health | Year: 2016

While whirling disease was first observed in Rainbow Trout Oncorhynchus mykiss in 1893, the complete life cycle of Myxobolus cerebralis (Mc), the causative agent of the disease, was not understood until 1984, when it was shown to involve two obligate hosts, a salmonid fish and the aquatic oligochaete Tubifex tubifex (Tt). The viability of the triactinomyxon (TAM) actinospores produced by Tt has been well studied, and is known to be temperature dependent and measured in days and weeks. Assertions that Mc myxospores produced by infected fish remain viable for years or even decades were made during the mid-20th century, decades before the Mc life cycle was described. Moreover, the duration of myxospore viability has not been well studied since the life cycle was elucidated. In a series of time-delay treatments, we assessed the long-term viability of Mc myxospores by exposure to Mc-susceptible Tt oligochaetes and quantified TAM production. As the time delay between inoculation and incubation of Mc myxospores in sand and water and exposure to Tt oligochaetes increased, TAM production decreased exponentially. Production among the 15-d time-delay replicates was reduced 74.7% compared with the 0-d treatment. Likewise, total TAM production was reduced 94.5, 99.4, and 99.9%, respectively, in the 90-, 120-, and 180-d time-delay treatments. Linear regression analysis of our data and the absence of TAM production among replicates of Mc myxospores held at 5◦C for 365 d prior to exposure to Mc-susceptible Tt oligochaetes indicate that the long-term viability of Mc myxospores is less than 1 year under the conditions of this study. © American Fisheries Society 2015. Source

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