Proliferative kidney disease of salmonid fish: a review

Clifton-Hadley, R. S.; Bucke, D.; Richards, R. H.

doi:10.1111/j.1365-2761.1984.tb01201.x

Cited by 68 publications

(47 citation statements)

References 20 publications

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“…In susceptible rainbow trout infected with a presumably non-pathogenic strain of C. shasta , parasites were identified in the presence of increased mucosal IgT antibody [24]. Although it is not known if this response is protective against C. shasta , protective antibody responses have been demonstrated in fish surviving other myxozoan infections [40, 41, 42, 43]. …”

Section: Discussionmentioning

confidence: 99%

Defenses of susceptible and resistant Chinook salmon (Onchorhynchus tshawytscha) against the myxozoan parasite Ceratomyxa shasta

Bjork¹,

Zhang²,

Hurst³

et al. 2014

Fish & Shellfish Immunology

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We investigated intra-specific variation in the response of salmon to infection with the myxozoan Ceratomyxa shasta by comparing the progress of parasite infection and measures of host immune response in susceptible and resistant Chinook salmon Oncorhynchus tshawytscha at days 12, 25 and 90 post exposure. There were no differences in invasion of the gills indicating that resistance does not occur at the site of entry. In the intestine on day 12, infection intensity and Ig+ cell numbers were higher in susceptible than resistant fish, but histological examination that timepoint showed more severe inflammation in resistant fish This suggests a role for the immune response in resistant fish that eliminates some parasites prior to or soon after reaching the intestine. Susceptible fish had a higher IFNγ, IL-6 and IL-10 response at day 12, but all died fatal enteronecrosis by day 25. The greatest fold change in IFNγ expression was detected at day 25 in resistant Chinook. In addition, the number of Ig+ cells in resistant Chinook also increased by day 25. By day 90, resistant Chinook had resolved the inflammation, cytokine expression had decreased and Ig+ cell numbers were similar to uninfected controls. Thus, it appears that the susceptible strain was incapable of containing or eliminating C. shasta but resistant fish: 1) reduced infection intensity during early intestinal infection 2) elicited an effective inflammatory response in the intestine that eliminated C. shasta 3) resolved the inflammation and recovered from infection.

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Section: Discussionmentioning

confidence: 99%

Defenses of susceptible and resistant Chinook salmon (Onchorhynchus tshawytscha) against the myxozoan parasite Ceratomyxa shasta

Bjork¹,

Zhang²,

Hurst³

et al. 2014

Fish & Shellfish Immunology

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“…The fish were fed daily and monitored for possible health impairment over 8 weeks. They were then killed by immersion in an 1/2500 aqueous solution of 2‐phenoxyethanol (Prolabo, Paris, France) and examined for PKD infection on the basis of nephromegaly scored according to Clifton‐Hadley et al . (1984) and splenomegaly, and for the presence of parasitic cells in kidney tissue imprints stained with May–Grünwald Giemsa, microscopically observed at ×200.…”

Section: Methodsmentioning

confidence: 99%

The persistence of infectivity of Tetracapsulabryosalmonae‐infected water for rainbow trout, Oncorhynchus mykiss (Walbaum)

Kinkelin

Forman

2002

Journal of Fish Diseases

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Proliferative kidney disease (PKD) is caused by the infection of susceptible salmonid fish with spores of the myxozoan Tetracapsula bryosalmonae, a parasite harboured and released by several species of bryozoans. Under natural conditions, PKD is a water‐borne infection of fish, whose outcome and spatio‐temporal dissemination depend on the viability of spores present in the water. In order to evaluate the duration of parasite infectivity, juvenile rainbow trout, Oncorhynchus mykiss, were exposed for 20 h to T. bryosalmonae‐infected water at various times post‐water collection or after different filtration procedures. When infected water was held in a temperature range of 14.5–17 °C for up to 14 days, PKD was transmitted to the fish only between 0 and 12 h post‐water collection and its infectivity vanished between 12 and 24 h. Similarly, the infectivity of water passed through 25 μm but not through 1 μm mesh filters, and was lost in the material eluted from the 1 μm filtration membrane although the parasite's DNA was amplified from this material. The parasitic infectivity in water appears to be fragile and this may offer opportunities to decrease the impact of PKD in trout farms by the implementation of management procedures aimed at reducing the number of the bryozoan‐holding surfaces located in the river, immediately upstream from these farms.

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“…In salmonids, the myxozoan Ceratomyxa shasta Noble, 1950 was found to infect fish between April and December (Hendrickson, Carleton and Manzer, 1989) and the related intestinal disease, ceratomyxosis, generally occurs at water temperatures above 10 xC (Palenzuela and Bartholomew, 2002). Similarly, the massive proliferation of extrasporogonic stages of Tetracapsuloides bryosalmonae Canning et al 2002, the cause of proliferative kidney disease (PKD) in salmonids, occurs only above 9 xC (Ferguson, 1981 ;Clifton-Hadley, Bucke and Richards, 1984). It has been suggested that the impact of temperature on the development of PKD primarily influences the kinetics of Tetracapsuloides multiplication in the host (Gay, Okamura and De Kinkelin, 2001) and similar conditions might apply for other myxozoan species in temperate climates.…”

Section: Introductionmentioning

confidence: 99%

Molecular studies on the seasonal occurrence and development of five myxozoans in farmed Salmo trutta L.

2005

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S U M M A R YFive myxozoan species, Tetracapsuloides bryosalmonae, Sphaerospora truttae, Chloromyxum schurovi, Chloromyxum truttae and a Myxobolus species were detected in farmed brown trout, Salmo trutta L. from Central Scotland. Using PCR and in situ hybridization, this study investigated the seasonal occurrence and tissue location of these species in young of the year brown trout. C. schurovi, C. truttae and Myxobolus sp. were first detected in brown trout in April, 2 months before T. bryosalmonae and S. truttae. T. bryosalmonae and S. truttae showed proliferation in the blood with intravascular stages of T. bryosalmonae accumulating in the heart. In contrast, only small amounts of PCR products of C. schurovi and C. truttae were obtained from the blood, suggesting that these species use the vascular system for transport but proliferate only in their target tissues from which large amounts of PCR product were obtained and where parasites were visible in histological sections. Large amounts of PCR product were obtained for T. bryosalmonae, S. truttae and both Chloromyxum species from the gills of brown trout, suggesting the gills as entry locus for these species. The neurotropic Myxobolus species formed plasmodia predominantly in the peripheral nerves, possibly indicating an entry route through the skin. Presporogonic stages of all other species had disappeared by September and mature spores were present from August onwards.

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Proliferative kidney disease of salmonid fish: a review

Cited by 68 publications

References 20 publications

Defenses of susceptible and resistant Chinook salmon (Onchorhynchus tshawytscha) against the myxozoan parasite Ceratomyxa shasta

Defenses of susceptible and resistant Chinook salmon (Onchorhynchus tshawytscha) against the myxozoan parasite Ceratomyxa shasta

The persistence of infectivity of Tetracapsulabryosalmonae‐infected water for rainbow trout, Oncorhynchus mykiss (Walbaum)

Molecular studies on the seasonal occurrence and development of five myxozoans in farmed Salmo trutta L.

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