Geographic and seasonal distribution of the infectious stage of Ceratomyxa shasta Noble, 1950, a myxozoan salmonid pathogen in the Fraser River system

1984 ◽  
Vol 62 (6) ◽  
pp. 1075-1080 ◽  
Author(s):  
Hilda Lei Ching ◽  
D. R. Munday

The infective stage of C. shasta was demonstrated to be present at two lower Fraser River sites. However, it was absent in the McGregor River, a tributary of the upper Fraser, and rarely present in the upper Fraser River near Prince George, B.C. Seasonally, the infective stage occurred in the lower Fraser River from late April to mid-November. In April 1983, 12% of 25 fish became infected with C. shasta, indicating a low onset of activity. In experiments in 1981, 10- and 20-day exposures of 216 juvenile chinook salmon resulted in increased infections of C. shasta, from 72 to 75% in May to 96 and 98% in July. Time to death decreased from a mean of 54 to 30 days from first exposure. In 1982, 5- and 10-day exposures resulted in deaths of 98% of 181 fish from August to November. Mean time to death increased from 27 to 48 days and was probably due to decreasing river temperatures. In November, 90% of the fish became infected at water temperatures of 4 – 6 °C.

1984 ◽  
Vol 62 (7) ◽  
pp. 1423-1424 ◽  
Author(s):  
Hilda Lei Ching

In a laboratory experiment conducted in the fall 1983, Oregon (Big Creek) and British Columbia (Capilano) hatchery Chinook salmon were exposed to Fraser River water containing the infectious stage of the myxozoan pathogen, Ceratomyxa shasta. The juvenile fish were exposed for 10 days in 370 L of water (74 L replaced every other day for 5 days). While only 1 of 21 Big Creek fish became infected, all 20 of the Capilano fish died of C. shasta within 40 days. The Big Creek fish demonstrated high resistance to the parasite while the Capilano fish had low resistance. These results were similar to those from field exposures in previous studies.


1984 ◽  
Vol 62 (6) ◽  
pp. 1081-1083 ◽  
Author(s):  
Hilda Lei Ching ◽  
D. R. Munday

Juvenile chinook salmon representing six stocks from the Fraser River drainage system were tested for susceptibility to the myxozoan pathogen, Ceratomyxa shasta. Of the six stocks tested, three were collected from the Nechako, Quesnel, and Clearwater rivers and three were hatchery stocks originating from Slim Creek and the Bowron and Birkenhead rivers. Of 302 fish exposed in August 1982, 95% became infected and died of ceratomyxosis. Susceptibility was high and time of death varied with the fish stock. High river temperatures during the 10 days of exposure and a high level of abundance of infectious C. shasta contributed to high mortalities of fish. Results of maintenance of infected fish in seawater indicated that ceratomyxosis is not attenuated and fish will continue to die after entering the estuarine environment.


1988 ◽  
Vol 23 (1) ◽  
pp. 100-113 ◽  
Author(s):  
I. H. Rogers ◽  
J. A. Servizi ◽  
C. D. Levings

Abstract Juvenile chinook salmon were sampled from August 1986 to March 1987 at stations near Prince George and Quesnel, influenced by sewage and pulp mill discharges. Maximum densities of 0.2 fish·mࢤ2 were recorded. Salmon were collected at reference sites in November 1986 and at Agassiz in April 1987. Fingerling chinook were exposed at 0.7°C to a commercial wood preservative containing 2,3,4,6 - tetrachlorophenol (TeCP) and pentachlorophenol (PCP) in the laboratory to simulate winter conditions in the upper Fraser River. Fish exposed for 62 days to 2 ug·Lࢤ1 contained a mean of 224 ng·gࢤ1 TeCP and 431 ng·gࢤ1 PCP. Chlorophenol uptake in feral fish was low. However, 3,4,5-trichloro-guaiacol levels to 304 ng·gࢤ1 and tetrachloroguaiacol values to 136 ng·gࢤ1 were measured in March. Fish from Agassiz, 518 km downstream of Quesnel, also contained these two substances. Thus chinook salmon can bioconcentrate persistent chlorophenols and chloroguaiacols directly from cold water (< 1°C). The biological consequences are uncertain.


2000 ◽  
Vol 57 (2) ◽  
pp. 405-413 ◽  
Author(s):  
J Y Wilson ◽  
R F Addison ◽  
D Martens ◽  
R Gordon ◽  
B Glickman

Juvenile chinook salmon (Oncorhynchus tshawytscha) were captured at six sites on the upper Fraser, Nechako, and Thompson rivers, British Columbia, Canada. Biological responses were measured in the liver to assess the effects of contaminants on the fish before they began migration downstream. Both ethoxyresorufin-O-deethylase (EROD) activity and CYP 1A concentrations were significantly enhanced, being two- to three-fold higher in Fraser River samples compared with those fish from reference sites on the Nechako River. DNA adduct concentrations were two- to four-fold higher in Fraser River fish, although liver histopathology appeared unaffected. Polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and polychlorinated biphenyls (PCBs) in the carcasses contributed to total contaminant burdens of less than 1 pg·g-1. Polycyclic aromatic hydrocarbon (PAH) metabolites were undetectable in nearly all samples of bile. There were strong correlations between EROD activity, CYP 1A induction, and DNA adduct concentrations but no clear correlation between these responses and PCDD, PCDF, or PCB concentrations.


FACETS ◽  
2018 ◽  
Vol 3 (1) ◽  
pp. 695-721 ◽  
Author(s):  
Krishna K. Thakur ◽  
Raphaël Vanderstichel ◽  
Shaorong Li ◽  
Emilie Laurin ◽  
Strahan Tucker ◽  
...  

Infectious diseases are likely contributing to large-scale declines in chinook salmon stocks in the Pacific Northwest, but the specific agents and diseases involved, and the prevalences in migratory salmon, are mostly unknown. We applied a high-throughput microfluidics platform to screen for 45 infectious agents in 556 out-migrating juvenile chinook salmon, collected from freshwater (FW) and saltwater (SW) locations in the Cowichan River system on Vancouver Island, Canada, during 2014. Nineteen agents (5 bacterial, 2 viral, and 12 parasitic) were detected, with prevalences ranging from 0.2% to 57.6%. Co-infections between Candidatus Branchiomonas cysticola Toenshoff, Kvellestad, Mitchell, Steinum, Falk, Colquhoun & Horn, 2012, Paranucleospora theridion Nylund, Nylund, Watanabe, Arnesen & Kalrsbakk, 2010, and gill chlamydia, all associated with gill disease, were observed in SW samples. We detected agents known to cause large-scale mortalities in Pacific salmon ( Ceratonova shasta (Noble, 1950), Parvicapsula minibicornis Kent, Whitaker & Dawe, 1977), and agents only recently reported in Pacific salmon in BC ( Ca. B. cysticola, P. theridion, Facilispora margolisi Jones, Prosperi-Porta & Kim, 2012 and Parvicapsula pseudobranchicola Karlsbakk, Saether, Hostlund, Fjellsoy & Nylund, 2002). Wild and hatchery fish were most divergent in agent profiles in FW, with higher agent diversity in wild fish. Differences in prevalence largely dissipated once they converged in the marine environment, although hatchery fish may be infected by a greater diversity of agents sooner after ocean entry by virtue of their more rapid migration from nearshore to offshore environments.


Author(s):  
Patricia Brandes ◽  
◽  
Brian Pyper ◽  
Michael Banks ◽  
David Jacobsen ◽  
...  

There are four distinct runs of Chinook Salmon (Oncorhynchus tshawytscha) in the Central Valley, named after their primary adult return times: fall, late-fall, winter, and spring run. Estimating the run-specific composition of juveniles entering and leaving the Sacramento–San Joaquin Delta is crucial for assessing population status and processes that affect juvenile survival through the Delta. Historically, the run of juvenile Chinook Salmon captured in the field has been determined using a length-at-date criteria (LDC); however, LDC run assignments may be inaccurate if there is high overlap in the run-specific timing and size of juveniles entering and leaving the Delta. In this study, we use genetic run assignments to assess the accuracy of LDC at two trawl locations in the Sacramento River (Delta entry) and at Chipps Island (Delta exit). Fin tissues were collected from approximately 7,500 juvenile Chinook Salmon captured in trawl samples between 2007 and 2011. Tissues were analyzed using 21 microsatellites to determine genetic run assignments for individuals, which we compared with LDC run assignments. Across years, there was extensive overlap among the distributions of run-specific fork lengths of genetically identified juveniles, indicating that run compositions based on LDC assignments would tend to underestimate fall-run and especially late-fall-run compositions at both trawl locations, and greatly overestimate spring-run compositions (both locations) and winter-run compositions (Chipps Island). We therefore strongly support ongoing efforts to include tissue sampling and genetic run identification of juvenile Chinook Salmon at key monitoring locations in the Sacramento–San Joaquin River system.


1985 ◽  
Vol 63 (7) ◽  
pp. 1737-1740 ◽  
Author(s):  
Susan M. Bower

Ceratomyxa shasta (mainly trophozoites) from the intestinal tract of a naturally infected juvenile chinook salmon (Oncorhynchus tshawytscha) developed in the coelom of laboratory-reared chinook salmon when inoculated intraperitoneally. All developmental stages were observed. Successful subpassages were accomplished by intraperitoneal inoculation of trophozoites and sporoblasts, but an infection did not develop when these stages were pipetted into the esophagus of susceptible fish. Heavy infections, including the presence of C. shasta sporoblasts or spores, were observed in 2 of 28 feral juvenile chinook salmon seined from the Fraser River estuary in late July and early August. Trophozoite-like cells were observed in six other chinook salmon from this group. No C. shasta were observed in 15 juvenile sockeye salmon (Oncorhynchus nerka) caught in the estuary along with the chinook salmon.


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