Monitoring Ceratomyxa shasta infection during a hatchery rearing cycle: Comparison of molecular, serological and histological methods

Department of Microbiology, Oregon State University, Corvallis, Oregon 97331-3804, USA.
Diseases of Aquatic Organisms (Impact Factor: 1.75). 11/2004; 62(1-2):85-92. DOI: 10.3354/dao062085
Source: PubMed


The prevalence of Ceratomyxa shasta infection in production stocks of steelhead Oncorhynchus mykiss and cutthroat trout O. clarki was monitored using a parasite-specific polymerase chain reaction (PCR) assay. For all 4 stocks of fish followed through their 1 yr rearing cycle, C. shasta infection was detected despite their genetic resistance to the disease and the treatment of the incoming water with ozone. Infection was confirmed using serological methods and standard histological procedures, except when prevalence was low (<10%). This suggests that at the lowest infection levels PCR is more sensitive than other methodologies, and can be used as an early indicator of infection. Results of the PCR assay continued to correlate with histological and serological detection as the numbers of parasites and the lesion severity increased over the rearing cycle. For both steelhead and cutthroat trout, early infections were characterized by large numbers of parasites on the epithelial surface, but with little associated inflammation. At release as yearlings, the infection prevalence in all stocks was greater than 90 % and the inflammatory response in many fish was extensive, with tissue necrosis and mucosal damage. Although C. shasta infections no longer result in high mortality at this facility, results of this study indicate that the parasite remains a contributor to low condition indices in these fish, despite their genetic resistance and ozone disinfection of the water supply.

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Available from: Jerri Bartholomew, Nov 24, 2015
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    • "Our study indicates that this occurs in the latter stages of infection, after proliferation in the blood. We also provide evidence that the presence of C. shasta trophozoites in the intestinal lumen of resistant fish (Bartholomew et al., 2004) is a result of migration through the intestine rather than a blocked site of entry as previously suggested. Previous studies also suggest that specific immunity may play a role (Bartholomew et al., 1989; Ibarra et al., 1991) and this remains unresolved. "
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    ABSTRACT: The myxozoan parasite Ceratomyxa shasta infects salmonids causing ceratomyxosis, a disease elicited by proliferation of the parasite in the intestine. This parasite is endemic to the Pacific Northwest of North America and salmon and trout strains from endemic river basins show increased resistance to the parasite. It has been suggested that these resistant fish (i) exclude the parasite at the site of invasion and/or (ii) prevent establishment in the intestine. Using parasites pre-labeled with a fluorescent stain, carboxyfluorescein succinimidyl diacetate (CFSE), the gills were identified as the site of attachment of C. shasta in a susceptible fish strain. In situ hybridization (ISH) of histological sections was then used to describe the invasion of the parasites in the gill filaments. To investigate differences in the progress of infection between resistant and susceptible fish, a C. shasta-susceptible strain of rainbow trout (Oncorhynchus mykiss) and a C. shasta-resistant strain of Chinook salmon (Oncorhynchus tshawytscha) were sampled at consecutive time points following exposure at an endemic site. Using ISH in both species, the parasite was observed to migrate from the gill epithelium into the gill blood vessels where replication and release of parasite stages occurred. Quantitative PCR verified entry of the parasite into the blood. Parasite levels in blood increased 4days p.i. and remained at a consistent level until the second week when parasite abundance increased further and coincided with host mortality. The timing of parasite replication and migration to the intestine were similar for both fish species. The field exposure dose was unexpectedly high and apparently overwhelmed the Chinook salmon's defenses, as no evidence of resistance to parasite penetration into the gills or prevention of parasite establishment in the intestine was observed.
    International journal for parasitology 04/2010; 40(9):1087-95. DOI:10.1016/j.ijpara.2010.03.005 · 3.87 Impact Factor
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    • "Therefore, once a fatal dose is acquired, additional parasites do not increase infection severity in terms of MDD. In this study, parasite severity is described only by MDD; histopathology (Bartholomew et al. 2004) and estimating myxospore abundance in affected fish could further clarify the effect of dose on the progress of infection. Parasite concentration significantly affected infection prevalence. "
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    ABSTRACT: Ceratomyxa shasta infects salmon and trout, causing ceratomyxosis, a disease characterized by parasite proliferation in the intestine and death. We used laboratory challenges to investigate the infective dose for 3 fish species: a susceptible strain of rainbow trout Oncorhynchus mykiss and comparatively resistant Chinook O. tshawytscha and coho salmon O. kisutch. For susceptible rainbow trout, we determined the outcome of infection under conditions of varying parasite dose, fish size, and parasite concentration. A single actinospore was sufficient to cause a lethal infection in susceptible rainbow trout. The mean days to death (MDD) did not significantly decrease among doses causing 100% prevalence, indicating a minimum time required for parasites to replicate to a fatal level. When dose was constant, but delivered in a higher parasite concentration, higher infection prevalence and mortality resulted. One actinospore fish(-1) caused 57% infection and mortality in fish challenged in 0.5 1 of water, whereas 10 spores fish(-1) resulted in an average of 49% infection and mortality in 1 l challenges. This effect is most likely due to a higher encounter rate in the smaller water volume. Neither infection prevalence nor MDD was significantly different between large trout (84.9 g) and small trout (6.3 g). Chinook salmon did not become infected even when challenged with 5000 actinospores. One fatal infection occurred in coho salmon challenged with 1000 actinospores. This study confirms that even low doses of C. shasta cause severe infection in highly susceptible fish, describes the dose response on MDD, and demonstrates that parasite concentration influences infection prevalence.
    Diseases of Aquatic Organisms 09/2009; 86(1):29-37. DOI:10.3354/dao02092 · 1.75 Impact Factor
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