Inter-Research > DAO > v48 > n2 > p125-131  
Diseases of Aquatic Organisms

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DAO 48:125-131 (2002)  -  doi:10.3354/dao048125

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

J. M. Ramsay1,*, D. J. Speare1, S. C. Dawe2, M. L. Kent2,**

1Department of Pathology and Microbiology, Atlantic Veterinary College, Charlottetown, Prince Edward Island C1A 4P3, Canada
2Pacific Biological Station, Fisheries and Oceans Canada, Nanaimo, British Columbia V9R 5K6, Canada
*E-mail: **Present address: Centre for Salmon Disease Research, Department of Microbiology, Oregon State University, Corvallis, Oregon 937331-3804, USA

ABSTRACT: 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

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