Loma salmonae‐associated growth rate suppression in rainbow trout, Oncorhynchus mykiss (Walbaum), occurs during early onset xenoma dissolution as determined by in situ hybridization and immunohistochemistry

Daley, J.; Markham, R. J. Frederick; Sheppard, Jo‐Ann I.; Beaman, H. J.; Sánchez, J. G.

doi:10.1046/j.1365-2761.1998.00112.x

Cited by 43 publications

(48 citation statements)

References 13 publications

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“…data). Beaman (1998) found that rainbow trout initially exposed to L. salmonae at lo\v temperatures (5 or 7°C) or at high temperature (21°C) did not develop xenomas, but were still protected following re-exposure at 15OC.…”

Section: Discussionmentioning

confidence: 94%

Resistance to reinfection in chinook salmon Oncorhynchus tshawytscha to Loma salmonae (Microsporidia)

Kent¹,

Dawe²

1999

Dis. Aquat. Org.

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Resistance to reinfection in chinook salmonOncorhynchus tshawytscha to Loma salmonae (Microsporidia) 'Fisheries and Oceans Canada, Pacific Biological Station, Nanaimo. British Columbia V9R 5K6. Canada '~e p a r t m e n t of Pathology and Microbiology, Atlantic Veterinary College. University of Prince Edward Island.Charlottetown, Prince Edward Island, Canada ABSTRACT: Chinook salmon Oncorhynchus tshawytscha were experimentally infected per OS with Loma salmonae and held in flow-through seawater tanks at 12 to 14'C. The fish exhibited 100% infection when first examined at 7 wk post initial exposure (p.e.), and by 20 wk p.e. they had completely recovered from gill infections. The recovered fish were then re-exposed the following week. All of these fish showed strong protection to new L. salmonaeinfections, while nai've fish exposed to the same inoculum developed the infection. Most of the re-exposed fish exhibited a few free spores or spores within phagocytes in the kidney interstitium at 20 to 29 wk p.e., but xenomas were not detected in either the gills or visceral organs. The kidney is the primary site of reticulo-endothelial activity, and thus these spores were likely deposited in the kidney by entrapment by fixed macrophages. It is possible that these spores provide immunologic stimuli to reinforce the resistance to new L. salmonae infections.

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Section: Discussionmentioning

confidence: 94%

Resistance to reinfection in chinook salmon Oncorhynchus tshawytscha to Loma salmonae (Microsporidia)

Kent¹,

Dawe²

1999

Dis. Aquat. Org.

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“…Reported effects of other parasitic infections on fish growth and condition have been mixed. For example, parasitic copepods have been reported to impair growth of Atlantic salmon (Birkeland 1996), whereas suppression of growth in Loma salmonae infected rainbow trout was only temporary (Speare et al 1998). In contrast, increased growth rates have resulted from infection with the tapeworm Schistocephalus solidus in laboratory-reared three-spined stickleback (Arnott et al 2000).…”

Section: Discussionmentioning

confidence: 99%

Parasite-associated mortality of juvenile Pacific salmon caused by the trematode Nanophyetus salmincola during early marine residence

Jacobson

Teel²,

Doornik³

et al. 2008

Mar. Ecol. Prog. Ser.

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The potential effect of the freshwater trematode Nanophyetus salmincola on early marine survival of Pacific salmon was assessed by monitoring the prevalence and intensity of metacercarial infection in yearling coho salmon Oncorhynchus kisutch, and yearling and subyearling Chinook salmon O. tshawytscha caught off Oregon and Washington during May, June, and September of 1999 to 2002. Annual prevalences of N. salmincola infection in yearling coho salmon were 62 to 78% and were significantly greater each year than in both yearling and subyearling Chinook salmon (19.3 to 53.8% and 40.5 to 53.5%, respectively). Yearling coho salmon also had significantly higher intensities of infection (from approximately 2-fold to 12-fold) than yearling and subyearling Chinook salmon. Prevalences and intensities in coho salmon caught in September were significantly lower (by approximately 21%) than in coho salmon caught in May or June in 3 of the 4 years. Variance to mean ratios of parasite abundance in coho salmon were also lowest in September, suggesting parasiteassociated host mortality during early ocean residence. There was no evidence for a seasonal decline in infection in yearling or subyearling Chinook salmon. Infection intensities, but not prevalences, were significantly greater in naturally produced (wild) coho salmon than in hatchery produced coho salmon and could be due to differences in exposure to the trematode. Highly infected naturally produced coho salmon were not caught in September. This study suggests that coho salmon with high intensities of N. salmincola may not survive early marine residence, and that disease processes need to be considered as a factor affecting marine survival of juvenile salmon.

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“…All fish were infected with Loma salmonae spores using gastric intubation, as described by Shaw et al (1998) and Speare et al (1998b). Gill tissue from L. salmonae-infected chinook, at Week 7 PE, was examined using sub-gross and standard histological techniques (Speare et al 1998a) to ensure the presence of branchial xenomas (containing spores) before intubation.…”

Section: Methodsmentioning

confidence: 99%

Xenoma formation during microsporidial gill disease of salmonids caused by Loma salmonae is affected by host species (Oncorhynchus tshawytscha, O. kisutch, O. mykiss) but not by salinity

Ramsay

Dawe²,

Kent³

2002

Dis. Aquat. Org.

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Host species and salinity often affect the development of disease in aquatic species. Eighty chinook salmon Oncorhynchus tshawytscha, 80 coho salmon O. kisutch and 80 rainbow trout O. mykiss were infected with Loma salmonae. Forty of each species were reared in seawater and 40 in freshwater. The mean number of xenomas per gill filament was 8 to 33 times greater in chinook salmon than in rainbow trout (RBT). Coho salmon had a mean xenoma intensity intermediate to that of chinook salmon and RBT. In contrast to the differences between species, salinity had no significant effect on xenoma intensity in any of these host species. The onset of xenoma formation occurred at Week 5 postexposure (PE) for chinook salmon and RBT, and at Week 6 PE for coho salmon. RBT had cleared all visible branchial xenomas by Week 9 PE, whereas xenomas persisted in coho and chinook salmon at Week 9 PE. Histologically, xenomas were visible in the filament arteries of the branchial arch in chinook and coho salmon gills but were absent from RBT gills. Fewer xenomas were seen in the central venous sinusoids of RBT than in chinook and coho salmon. The lower xenoma intensity, shorter duration of infection and pathological characteristics, common to microsporidial gill disease in RBT, suggest a degree of resistance to clinical disease that is not seen in coho and chinook salmon.KEY WORDS: Loma salmonae · Host species · Salinity · Xenoma formation · Xenoma intensity Resale or republication not permitted without written consent of the publisher

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Loma salmonae‐associated growth rate suppression in rainbow trout, Oncorhynchus mykiss (Walbaum), occurs during early onset xenoma dissolution as determined by in situ hybridization and immunohistochemistry

Cited by 43 publications

References 13 publications

Resistance to reinfection in chinook salmon Oncorhynchus tshawytscha to Loma salmonae (Microsporidia)

Resistance to reinfection in chinook salmon Oncorhynchus tshawytscha to Loma salmonae (Microsporidia)

Parasite-associated mortality of juvenile Pacific salmon caused by the trematode Nanophyetus salmincola during early marine residence

Xenoma formation during microsporidial gill disease of salmonids caused by Loma salmonae is affected by host species (Oncorhynchus tshawytscha, O. kisutch, O. mykiss) but not by salinity

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