Myxobolus cerebralis causes pre‐sporogonic mortality in juvenile Mountain Whitefish ( Prosopium williamsoni )

Author(s):  
Benjamin Americus ◽  
George Schisler ◽  
Jerri L Bartholomew ◽  
Stephen D Atkinson





1985 ◽  
Vol 63 (2) ◽  
pp. 396-399 ◽  
Author(s):  
Hilda Lei Ching

As a result of experimental infections in chicks, diplostomula found in the retina of chinook salmon from the Nechako River were identified as Diplostomum (Diplostomum) baeri bucculentum. Eyeflukes in other salmonids were considered to be the same species based on similar measurements and site in the eyes. These eyeflukes varied in prevalence and mean intensity in seven salmonid species surveyed in nine localities in 1979–1981. The following fish were sampled: rainbow trout (Salmo gairdneri), 505; mountain whitefish (Prosopium williamsoni), 334; lake whitefish (Coregonus clupeaformis), 32; Dolly Varden (Salvelinus malma), 66; lake trout (S. namaycush), 13; kokanee or sockeye salmon (Oncorhynchus nerka), 323; and chinook salmon (O. tshawytscha), 164. Eyeflukes had prevalences ranging from 84 to 100% in six lakes, 64% in the river, 53% in one reservoir site, and a prevalence of 15% in the other reservoir site. Mountain and lake whitefishes had high mean intensities while kokanee had low mean intensities. Correlation of increased intensity with increased fish size was significant for 6 of 27 samples. Four samples of lake whitefish, mountain whitefish, rainbow trout, and chinook salmon showed significant asymmetry when numbers of diplostomula were compared between eyes. More of the heavily infected fish showed asymmetry than did the lightly infected fish.





2002 ◽  
Vol 51 ◽  
pp. 113-121 ◽  
Author(s):  
KA Beauchamp ◽  
M Gay ◽  
GO Kelley ◽  
M El-Matbouli ◽  
RD Kathman ◽  
...  


2018 ◽  
Vol 30 (4) ◽  
pp. 264-279 ◽  
Author(s):  
R. Barry Nehring ◽  
John Alves ◽  
Joshua B. Nehring ◽  
Benjamin Felt




<EM>ABSTRACT. </EM>Anadromous fish were excluded above Pelton Round Butte Hydroelectric Project (PRB Project), located midway (RM 100) on the Deschutes River in central Oregon, beginning in 1968. Reintroduction of these fish above the PRB Project is proposed to meet conservation concerns that arise from lack of natural production and separation of populations. One consideration, when moving fish groups that have been isolated one from the other for thirty years, is that of disease. The health of the fish populations above Round Butte Dam could be seriously jeopardized by the introduction of whirling disease. Straying hatchery steelhead trout <em>Oncorhynchus mykiss </em>were detected with <em>Myxobolus cerebralis </em>spores, in 1987, at Warm Springs National Fish Hatchery, below the PRB Project. <em>Myxobolus cerebralis </em>is established in tributaries of the upper Columbia River basin and of the Snake River basin, where some of these straying hatchery and wild steelhead trout may have originated. From 1997 to 2000, fish from the Deschutes River basin have been sampled for the presence of <em>M. cerebralis</em>. The parasite has been found in both straying hatchery and unmarked adult chinook salmon <em>O. tshawytscha </em>and steelhead trout. Presently there is no evidence of infection of resident fish or in returning adult fish originating from Round Butte Hatchery, although the potential for establishment of <em>M. cerebralis </em>in the Deschutes River watershed cannot be ruled out.



<em>ABSTRACT. Myxobolus cerebralis </em>possesses unique phenotypic and genotypic characteristics when compared with other histozoic parasites from the phylum Myxozoa. The parasite infects the cartilage and thereby induces a serious and potentially lethal disease in salmonid fish. Comparisons of the small subunit ribosomal DNA (ssu rDNA) sequences of <em>M. cerebralis </em>to other myxozoans demonstrate that the parasite has evolved separately from other <em>Myxobolus </em>spp. that may appear in cartilage or nervous tissues of the fish host. <em>Myxobolus cerebralis </em>has a complex life cycle involving two hosts and numerous developmental stages that may divide by mitosis, endogeny, or plasmotomy, and, at one stage, by meiosis. In the salmonid host, the parasite undergoes extensive migration from initial sites of attachment to the epidermis, through the nervous system, to reach cartilage, the site where sporogenesis occurs. During this migration, parasite numbers may increase by replication. Sporogenesis is initiated by autogamy, a process typical of pansporoblastic myxosporean development that involves the union of the one cell (pericyte) with another (sporogonic). Following this union, the sporogonic cell will give rise to all subsequent cells that differentiate into the lenticular shaped spore with a diameter of approximately 10 µm. This spore or myxospore is an environmentally resistant stage characterized by two hardened valves surrounding two polar capsules with coiled filaments and a binucleate sporoplasm cell. In the fish, these spores are found only in cartilage where they reside until released from fish that die or are consumed by other fish or fish-eating animals (e.g., birds). Spores reaching the aquatic sediments can be ingested and hatch in susceptible oligochaete hosts. The released sporoplasm invades and then resides between cells of the intestinal mucosa. In contrast to the parasite in the fish host, the parasite in the oligochaete undergoes the entire developmental cycle in this location. This developmental cycle involves merogony, gametogamy or the formation of haploid gametes, and sporogony. The actinosporean spores, formed at the culmination of this development, are released into the lumen of the intestine, prior to discharging into the aquatic environment. The mechanisms underlying the complex development of <em>M. cerebralis</em>, and its interactions with both hosts, are poorly understood. Recent advances, however, are providing insights into the factors that mediate certain phases of the infection. In this review, we consider known and recently obtained information on the taxonomy, development, and life cycle of the parasite.



<em>Abstract.</em>—Laboratory challenges of two rainbow trout <em>Oncorhynchus mykiss </em>strains with <em>Myxobolus cerebralis </em>triactinomyxons confirm the resistance to whirling disease of the Hofer trout strain. Although the number of fish that became infected and developed clinical disease was similar for the Hofer and the Trout Lodge strains at all challenge doses, the median spore numbers were lower at all challenge doses for the Hofer rainbow trout. Parasite challenge doses required to produce lesions of high severity were 10-fold lower for the Trout Lodge strain (100 triactinomyxons) than the Hofer strain (1,000 triactinomyxons). Challenges of the Hofer strain with other common salmonid pathogens; the myxozoans <em>Ceratomyxa shasta </em>and <em>Tetracapsuloides bryosalmonae</em>, the bacterium <em>Yersinia ruckeri</em>, and the viruses Salmonid herpes-like virus type 1 and infectious hematopoietic necrosis virus demonstrate that the susceptibility of the Hofer strain was similar to what would be expected for other strains of rainbow trout, either domestic or wild. These pathogen challenges provide evidence that the Hofer trout present a low risk for introducing any pathogen that might be detrimental to native or established fish populations or further amplifying those that are endemic.



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